{In addition, the level of HES1 mRNA remained constant irrespective of the presence or absence of either synthetic miR-23 or mutant miR-23 (Fig. 2c).These results further suggest that synthetic miR-23 might suppress the expression of the gene for Hes1 at the translational level.}{Moreover, the level of HES1 mRNA was unaffected by synthetic siRNA-miR-23 (Fig. 2g).These results indicate that synthetic siRNA-miR-23 interfered with the function of miR-23 and, as a result, it promoted the accumulation of Hes1 protein. These results strengthen our hypothesis that miR-23 regulates the expression of Hes1 at the post-transcriptional level.}
{The mRNA levels from the miR-32-resistant virus (PFV-1D32) were three times as high as those from the unmodified virus, consistent with the anti-miR-32 results (Fig. 2, E and C). Therefore, miR-32 exerts a direct, sequence-specific effect against PFV-1.}
{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3B and C).}{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3B and C).}
{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3B and C).}{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3B and C).}
{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}
{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}
{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}
{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}{Segments from all three UTRs imparted miR-196-dependent repression to the luciferase reporter without a substantial decrease in reporter mRNA, indicating predominantly translational inhibition (Fig. 3, B and C).}
{By analyzing RNA isolated from the mouse,the HOXB8 5'-RACE results validated this miRNA-target interaction in the animal, whereas previous experimental support for predicted mammalian miRNA targets has come from reporter assays in cultured cells (11).The vertical arrowhead indicates the 5' end of cleavage products detected by 5'-RACE, with the frequency of clones noted. Hs, human; Mm, mouse; Rn, rat;Xl, frog; Dr, zebrafish; Fr, pufferfish.}
{On the other hand, there was no difference in the mRNA expression levels of BCL6 before and after treatment as examined by conventional RT-PCR (Figure 6A) and quantitative real-time RT-PCR (data not shown),suggesting translational inhibition of BCL6 by treatment and not mRNA degradation.}{On the other hand, there was no difference in the mRNA expression levels of BCL6 before and after treatment as examined by conventional RT-PCR (Figure 6A) and quantitative real-time RT-PCR (data not shown),suggesting translational inhibition of BCL6 by treatment and not mRNA degradation.}
{In these experiments we were able to show by quantitative RT-PCR that the action of the miR-122 on the reporter was primarily at the level of mRNA-degradation.}
{In these experiments we were able to show by quantitative RT-PCR that the action of the miR-122 on the reporter was primarily at the level of mRNA-degradation.}
{In these experiments we were able to show by quantitative RT-PCR that the action of the miR-122 on the reporter was primarily at the level of mRNA-degradation.}
{We haveevaluated mRNA levels by amplifying BCL2 cDNA from cells transfected with the pSR-miR-15_16-WT or with specific miR-15a and miR-16-1 RNA oligos by RT-PCR. No differences in the levels of BCL2 expression were observed between any of these samples and control cells (untransfected or transfected with the empty vector) (Fig. 2B). This result demonstrates that miR-15a and miR-16-1 do not affect mRNA stability and regulate Bcl2 expression at the posttranscriptional level.}
{We haveevaluated mRNA levels by amplifying BCL2 cDNA from cells transfected with the pSR-miR-15_16-WT or with specific miR-15a and miR-16-1 RNA oligos by RT-PCR. No differences in the levels of BCL2 expression were observed between any of these samples and control cells (untransfected or transfected with the empty vector) (Fig. 2B). This result demonstrates that miR-15a and miR-16-1 do not affect mRNA stability and regulate Bcl2 expression at the posttranscriptional level.}
The enforced expression of both miRs also induced a clear reduction of kit protein level (Fig. 5A Middle). Here again, no significant modulation of kit mRNA was observed by real-time PCR (data not shown).
{The enforced expression of both miRs also induced a clear reduction of kit protein level (Fig. 5A Middle). Here again, no significant modulation of kit mRNA was observed by real-time PCR (data not shown).}
{A significant reduction at themRNAand protein levels for HOXA1 was found for K562 cells transfected with the miR-10a precursor but not with the negative control (Fig. 3 F and G). These data indicate that miR-10a targets HOXA1 in vitro and in vivo.}
{As expected, AIB1 mRNA levels were unaffected by Mir-17-5p (Fig. 2A), although Northern blotting (Fig. 2A) and real-time PCR (data not shown) revealed that AIB1 mRNA was sharply reduced by cotransfection of an AIB1- specific short interfering RNA (siRNA) molecule. }
{As expected, AIB1 mRNA levels were unaffected by Mir-17-5p (Fig. 2A), although Northern blotting (Fig. 2A) and real-time PCR (data not shown) revealed that AIB1 mRNA was sharply reduced by cotransfection of an AIB1- specific short interfering RNA (siRNA) molecule. }
{To investigate whether miR-155 targeted hAT1R mRNA for degradation, real-time PCR experiments were performed on RNA isolated from transfected hPFB cells. These data demonstrated that cells transfected with miR-155 did not significantly decreasehAT1R steady statemRNAlevels (Fig. 3B).}
{As shown in the Western blots of Fig. 2B, ERBB2 protein levels were reduced to 40 and 65% that of control (SKBR3-puro) levels in SKBR3-125a and SKBR3-125b cells, respectively, whereas ERBB3 protein levels were reduced to 60 and 80% that of control levels, respectively, after loading normalization by _-actin levels.}
{As shown in the Northern blots of Fig. 2A, ERBB2 transcript levels in the SKBR3-125a and SKBR3-125b cells were 52 and 80%, respectively, of SKBR3-puro control levels after loading normalization by glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA levels. Likewise, ERBB3 mRNA levels in SKBR3-125a and SKBR3-125b cells were 67 and 90%, respectively, that of SKBR3-puro control levels after normalization.}
{As shown in the Northern blots of Fig. 2A, ERBB2 transcript levels in the SKBR3-125a and SKBR3-125b cells were 52 and 80%, respectively, of SKBR3-puro control levels after loading normalization by glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA levels. Likewise, ERBB3 mRNA levels in SKBR3-125a and SKBR3-125b cells were 67 and 90%, respectively, that of SKBR3-puro control levels after normalization.}
{As shown in the Northern blots of Fig. 2A, ERBB2 transcript levels in the SKBR3-125a and SKBR3-125b cells were 52 and 80%, respectively, of SKBR3-puro control levels after loading normalization by glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA levels. Likewise, ERBB3 mRNA levels in SKBR3-125a and SKBR3-125b cells were 67 and 90%, respectively, that of SKBR3-puro control levels after normalization.}
{Because we did not observe an miR132-induced reduction in p250GAPmRNA(data not shown), we suggest that miR132 regulates p250GAP by a translational block.}
{We then confirmed that exogenous miR-192 (Mimic) can reduce endogenous SIP1 mRNA expression (Fig. 4F), suggesting that miR-192 reduces the expression of its target SIP1 most likely via mRNA degradation.}{We then confirmed that exogenous miR-192 (Mimic) can reduce endogenous SIP1 mRNA expression (Fig. 4F), suggesting that miR-192 reduces the expression of its target SIP1 most likely via mRNA degradation.}
Co-transfection of these plasmids with miR-17-5p or miR-20a antisense oligonucleotides, but not scrambled oligonucleotides, enhanced expression of the sensor constructs, indicating inhibition of these miRNAs (Fig. 4a). Because of nucleotide similarity between miR-17-5p and miR-20a, both were inhibited by antisense oligonucleotides directed against either miRNA. Transfection with miR-17-5p and miR-20a antisense oligonucleotides, but not scrambled oligonucleotides, resulted in an approximately fourfold increase in E2F1 protein levels without altering E2F1 mRNA abundance (Fig. 4b, c).
{Western blots of transgenic heart protein overexpressing miR-1 postnatally showed a significant decrease in Hand2 protein levels compared with non-transgenic littermates, confirming Hand2 as a miR-1 target in vivo (Fig. 4e). No change in mRNA levels of Hand2 was noted (Fig. 4e).}
{By contrast,the mRNA levels of SRF and HDAC4 were not alterer by these miRNAs(Fig.4d),supporting the notion that miRNA repress the function of their target genes}{The application of 2'-O-methyl-antisense oligobibonucleotides targeted towards miR-1 or miR-133 relieved the repression ot HDAC4 or SRF protein, respectively(Fig-4g),but had no effect on their mRNA levels(Fig.4f)}
{By contrast,the mRNA levels of SRF and HDAC4 were not alterer by these miRNAs(Fig.4d),supporting the notion that miRNA repress the function of their target genes}{The application of 2'-O-methyl-antisense oligobibonucleotides targeted towards miR-1 or miR-133 relieved the repression ot HDAC4 or SRF protein, respectively(Fig-4g),but had no effect on their mRNA levels(Fig.4f)}
{By contrast,the mRNA levels of SRF and HDAC4 were not alterer by these miRNAs(Fig.4d),supporting the notion that miRNA repress the function of their target genes}{The application of 2'-O-methyl-antisense oligobibonucleotides targeted towards miR-1 or miR-133 relieved the repression ot HDAC4 or SRF protein, respectively(Fig-4g),but had no effect on their mRNA levels(Fig.4f)/}
{By contrast,the mRNA levels of SRF and HDAC4 were not alterer by these miRNAs(Fig.4d),supporting the notion that miRNA repress the function of their target genes}{The application of 2'-O-methyl-antisense oligobibonucleotides targeted towards miR-1 or miR-133 relieved the repression ot HDAC4 or SRF protein, respectively(Fig-4g),but had no effect on their mRNA levels(Fig.4f)/}
{Because miRNAs can also downregulate a specific target by affecting mRNA stability1, we investigated the effects of miR-1 on the expression of the mRNA for GJA1 and KCNJ2. We found that miR-1 had no apparent effects on the mRNA stability of these genes (Fig. 2e).}
{Because miRNAs can also downregulate a specific target by affecting mRNA stability1, we investigated the effects of miR-1 on the expression of the mRNA for GJA1 and KCNJ2. We found that miR-1 had no apparent effects on the mRNA stability of these genes (Fig. 2e).}
{Using quantitative RT-PCR and immunoblot analysis, we observed a 2-fold effect on LATS2 RNA levels and 4- to 5- fold on protein levels by the miR-371-3 cluster (Figure 5C).As a control, we used a LATS2 knockdown construct (Figure 5F). These results show that a combined effect of RNA destruction and translation inhibition is used by miR-372&3 to silence LATS2.}
{Using quantitative RT-PCR and immunoblot analysis, we observed a 2-fold effect on LATS2 RNA levels and 4- to 5- fold on protein levels by the miR-371-3 cluster (Figure 5C).As a control, we used a LATS2 knockdown construct (Figure 5F). These results show that a combined effect of RNA destruction and translation inhibition is used by miR-372&3 to silence LATS2.}
{Since miRNAs can repress protein production by affecting either mRNA stability or translation, we assessed both mRNA and protein levels in miR-1-2 mutant hearts. qPCR revealed a nearly 2-fold increase in Irx5 mRNA levels in miR-1-2-null hearts compared to wild-type, and western blots showed an approximately 5-fold increase in Irx5 protein accumulation by densitometry (Figure 4).}
{The mRNA levels of Hand2 were unchanged in miR-1-2 mutants, but the protein levels were increased approximately 4-fold as seen by western blots (Figure 3),consistent with Hand2 being a physiologic miR-1 target in vivo.}
{RT-PCR assays reveal that expression of miR-124, but not miR-124-mt, reduces SCP1 and induces proneural bHLH factors Ngn2 and NeuroD and neuronal marker TuJ.}
{RT-PCR assays reveal that expression of miR-124, but not miR-124-mt, reduces SCP1 and induces proneural bHLH factors Ngn2 and NeuroD and neuronal marker TuJ.}
{RT-PCR assays reveal that expression of miR-124, but not miR-124-mt, reduces SCP1 and induces proneural bHLH factors Ngn2 and NeuroD and neuronal marker TuJ.}
{By comparison, miR-133 produced marginal reduction of KCNQ1 mRNA level (Fig. 4F), indicating that miR-133 does not affect KCNQ1 mRNA stability}
{By comparison, miR-133 produced marginal reduction of KCNQ1 mRNA level (Fig. 4F), indicating that miR-133 does not affect KCNQ1 mRNA stability}
{By comparison, miR-133 produced marginal reduction of KCNQ1 mRNA level (Fig. 4F), indicating that miR-133 does not affect KCNQ1 mRNA stability}
{By comparison, miR-133 produced marginal reduction of KCNQ1 mRNA level (Fig. 4F), indicating that miR-133 does not affect KCNQ1 mRNA stability}
{The KCNE1 mRNA was unaffected by miR-1 (Fig. 5F).}
{The KCNE1 mRNA was unaffected by miR-1 (Fig. 5F).}
{The KCNE1 mRNA was unaffected by miR-1 (Fig. 5F).}
{Using CDK6 Western blot analyses, we observed that whereas the original HCT-116 cells with miR-124a methylation-associated silencing strongly expressed CDK6, the cells treated with the demethylating agent or the DKO cells showed CDK6 down-regulation (Fig. 3A). On the other hand, there was no difference in the CDK6 mRNA expression levels in any of the described cells (Fig. 3A), suggesting translational inhibition of CDK6 by miR-124a, rather than mRNA degradation or transcriptional repression.}{Western blots for CDK6 in original HCT-116 cells and HCT-116 cells transfected with miR-124a precursor, showing CDK6 down-regulation. RT-PCR analyses of CDK6 mRNA do not show any change.}
{We subsequently investigated the effects of the miRNAs on mRNA levels of HSP60, HSP70 and Casp9 in H9c2 cells. The mRNA levels of HSP60, HSP70 were unaffected by miR-1, indicating that miR-1 and miR-133 do not affect their mRNA stability.}
{We subsequently investigated the effects of the miRNAs on mRNA levels of HSP60, HSP70 and Casp9 in H9c2 cells. The mRNA levels of HSP60, HSP70 were unaffected by miR-1, indicating that miR-1 and miR-133 do not affect their mRNA stability.}
{[assessed from the northern blot picture in the paper]}
{[assessed from the northern blot picture in the paper]}
{[assessed from the northern blot picture in the paper]}
{[assessed from the northern blot picture in the paper]}
{[assessed from the northern blot picture in the paper]}
{[assessed from the northern blot picture in the paper]}
{The results illustrated in Figure 3A and B clearly demonstrated that the miRNA-masking antisense ODNs specifically increased the protein level of HCN2 and HCN4 by _70 and _45%, respectively, without affecting the transcript}
{The results illustrated in Figure 3A and B clearly demonstrated that the miRNA-masking antisense ODNs specifically increased the protein level of HCN2 and HCN4 by _70 and _45%, respectively, without affecting the transcript}
{The results illustrated in Figure 3A and B clearly demonstrated that the miRNA-masking antisense ODNs specifically increased the protein level of HCN2 and HCN4 by _70 and _45%, respectively, without affecting the transcript}
{RT-qPCR analyses revealed an _1.6-fold (p < 0.005) increase in PTBP1 mRNA from the anti-miR-124-transfected cells as compared to the anti-miR-1-transfected control (Figure 6E).}
{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}
{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}
{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}
{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}
{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}
{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}{By comparison, miR-133 produced virtually no effects on HERG mRNA level (Fig. 2D), indicating that miR-133 does not affect HERG mRNA stability.}
{[accessed from the pictures]}{[accessed from the pictures]}
{The steady-state levels of the reporter gene mRNA were unaffected by miR-134 overexpression, suggesting that the observed effect of miR-134 on luciferase expression does not reflect a change in the stability of the luciferase mRNA (Supplementary Fig. 6c).}
{In contrast, si-miR-neg-transfected cells showed no reduction in Fos activation. Because inhibition of expression by miRNAs may also be mediated by mRNA degradation (30, 31), we examined whether the PMA-induced elevation in Fos mRNA levels might be affected by si-miR-7b. Fig. 4B shows that mRNA expression is not changed, indicating that reduction of Fos levels by miR-7b occurs by translational suppression rather than by mRNA degradation.}
{In contrast, si-miR-neg-transfected cells showed no reduction in Fos activation. Because inhibition of expression by miRNAs may also be mediated by mRNA degradation (30, 31), we examined whether the PMA-induced elevation in Fos mRNA levels might be affected by si-miR-7b. Fig. 4B shows that mRNA expression is not changed, indicating that reduction of Fos levels by miR-7b occurs by translational suppression rather than by mRNA degradation.}
{miR-206 alone is suffi cient to decrease Pola1 at the mRNA and protein levels as early as 24 h after transfection (Fig. 4 A). During differentiation of MBs to MTs, Pola1 mRNA and protein were also decreased (Fig. 4 A).}{The Pola1 promoter requires the activity of E2F, a transcription factor that is repressed by pRb during myogenesis (Kalma et al., 2001; Kitzmann and Fernandez, 2001), so we wondered how much of the down- regulation of Pola1 mRNA during differentiation was dependent on miR-206. Antisense to miR-206 signifi cantly delayed the down-regulation of Pola1 mRNA (Fig. 4 D).}
{miR-206 alone is suffi cient to decrease Pola1 at the mRNA and protein levels as early as 24 h after transfection (Fig. 4 A). During differentiation of MBs to MTs, Pola1 mRNA and protein were also decreased (Fig. 4 A).}{The Pola1 promoter requires the activity of E2F, a transcription factor that is repressed by pRb during myogenesis (Kalma et al., 2001; Kitzmann and Fernandez, 2001), so we wondered how much of the down- regulation of Pola1 mRNA during differentiation was dependent on miR-206. Antisense to miR-206 signifi cantly delayed the down-regulation of Pola1 mRNA (Fig. 4 D).}
{Transcriptional activity of Pola1 was too low to be measured by nuclear run-on (unpublished data), but that of B-ind1 was measured and found to not decrease after C2C12 differentiation or after the introduction of miR-1 and -206 (Fig. 7 D). The Northern blots that accompanied this experiment show that the steady-state mRNA level of B-ind1 is repressed by at least fi vefold (Fig. 7 D), suggesting that the miRNAs repress B-ind1 at the posttranscriptional level.}{B-ind1 might infl uence differentiation through its interaction with the G protein Rac-1. Down-regulation of B-ind1 mRNA was inversely related to the up-regulation of miR-206 during differentiation and was abrogated when miR-206 was inhibited by anti-miR-206 (Fig. 6 E).}
{Transcriptional activity of Pola1 was too low to be measured by nuclear run-on (unpublished data), but that of B-ind1 was measured and found to not decrease after C2C12 differentiation or after the introduction of miR-1 and -206 (Fig. 7 D). The Northern blots that accompanied this experiment show that the steady-state mRNA level of B-ind1 is repressed by at least fi vefold (Fig. 7 D), suggesting that the miRNAs repress B-ind1 at the posttranscriptional level.}{B-ind1 might infl uence differentiation through its interaction with the G protein Rac-1. Down-regulation of B-ind1 mRNA was inversely related to the up-regulation of miR-206 during differentiation and was abrogated when miR-206 was inhibited by anti-miR-206 (Fig. 6 E).}
{Three lines of evidence suggest that misregulation of expanded contributes to the lean phenotype of miR-278 mutants. expanded mRNA levels increased several fold in miR-278 mutant tissues (Fig. 5A).}
{Three lines of evidence suggest that misregulation of expanded contributes to the lean phenotype of miR-278 mutants. expanded mRNA levels increased several fold in miR-278 mutant tissues (Fig. 5A).}
{The gfp::lin41 30-UTR mRNA levels remained unaffected, whereas GFP protein levels were dramatically reduced upon let-7 overexpression (Figure 3C).}
{The gfp::lin41 30-UTR mRNA levels remained unaffected, whereas GFP protein levels were dramatically reduced upon let-7 overexpression (Figure 3C).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{Moreover, the level of Hesl mRNA was unaffected by synthetic siRNA-miR-23.}
{The NFIB mRNA levels were unchanged between the two transfectants (Fig. 3a), suggesting that repression of NFIB by miR-21 is mainly caused by translational suppression.}
{The PDCD4 mRNA level did not change significantly, that is, o10%, in cells transfected with the anti-miR-21 compared to the negative control (Figure 2a), suggesting that the reduction in Pdcd4 protein is likely a result of translational inhibition.}
{This analysis revealed that stable expression of miR-148a in HeLa cells resulted in small but significant reduction (P < 0.001) inDnmt3b1mRNA levels of 25%, while no reduction in Dnmt3b3 mRNA levels was observed (Fig. 3A). Thus, the expression of miR-148a affects the mRNA stability of Dnmt3b1, but not Dnmt3b3, leading to a relative increase in the abundance of Dnmt3b3 compared with Dnmt3b1 and all other Dnmt3b splice variants that express the targeted site.}
{This analysis revealed that stable expression of miR-148a in HeLa cells resulted in small but significant reduction (P < 0.001) inDnmt3b1mRNA levels of 25%, while no reduction in Dnmt3b3 mRNA levels was observed (Fig. 3A). Thus, the expression of miR-148a affects the mRNA stability of Dnmt3b1, but not Dnmt3b3, leading to a relative increase in the abundance of Dnmt3b3 compared with Dnmt3b1 and all other Dnmt3b splice variants that express the targeted site.}
{Despite the pre-senescent phenotype of these cells and their high p16 levels, miR-24 overexpression (Fig. 4A, right) markedly reduced p16 protein abundance (Fig. 4B), but not p16 mRNA levels (Fig. 4A, left).}{Conversely, Y HDFs were transfected with AS-miR-24 in order to reduce the function of miR-24 in these populations with high endogenous miR-24 levels (Fig. 3A). The intervention to reduce miR-24 (Fig. 4C, right) caused no significant changes in p16 mRNA levels (Fig. 4C, left), but it strongly increased p16 protein abundance (Fig. 4D).}{By 48 hr after transfection, the expression of both EGFP and EGFP-p16 mRNAs remained unchanged as a function of AS-miR-24 (Supplemental Fig. S7). }
{Despite the pre-senescent phenotype of these cells and their high p16 levels, miR-24 overexpression (Fig. 4A, right) markedly reduced p16 protein abundance (Fig. 4B), but not p16 mRNA levels (Fig. 4A, left).}{Conversely, Y HDFs were transfected with AS-miR-24 in order to reduce the function of miR-24 in these populations with high endogenous miR-24 levels (Fig. 3A). The intervention to reduce miR-24 (Fig. 4C, right) caused no significant changes in p16 mRNA levels (Fig. 4C, left), but it strongly increased p16 protein abundance (Fig. 4D).}{By 48 hr after transfection, the expression of both EGFP and EGFP-p16 mRNAs remained unchanged as a function of AS-miR-24 (Supplemental Fig. S7). }
{However, E2F1 mRNA decreased by 2-fold upon miR-106b and miR-93 transfection, possibly because of partial mRNA degradation or downmodulation of E2F1 transcriptional activators (Figure 3F).}
{However, E2F1 mRNA decreased by 2-fold upon miR-106b and miR-93 transfection, possibly because of partial mRNA degradation or downmodulation of E2F1 transcriptional activators (Figure 3F).}
{In fact, their inhibition by ASOs enhanced the expression of p21 protein (Figure 4A). Conversely, upregulation of miR-106b and miR-93 achieved by either oligonucleotides transfection (Figure 4B) or lentiviral transduction (Figure 4C) repressed p21 protein expression without significant changes in p21 mRNA levels (Figure 4D).}
{In fact, their inhibition by ASOs enhanced the expression of p21 protein (Figure 4A). Conversely, upregulation of miR-106b and miR-93 achieved by either oligonucleotides transfection (Figure 4B) or lentiviral transduction (Figure 4C) repressed p21 protein expression without significant changes in p21 mRNA levels (Figure 4D).}
{Our observations that increased miR-224 reduced the endogenous API-5 mRNA levels in cells thus suggest that it is likely that miR-224 inhibit API-5 expression at the posttranscriptional level by degrading API-5 transcript resulting in reduced steady-state API-5 transcript levels (Fig. 3E).}
{Our observations that increased miR-224 reduced the endogenous API-5 mRNA levels in cells thus suggest that it is likely that miR-224 inhibit API-5 expression at the posttranscriptional level by degrading API-5 transcript resulting in reduced steady-state API-5 transcript levels (Fig. 3E).}
{Our observations that increased miR-224 reduced the endogenous API-5 mRNA levels in cells thus suggest that it is likely that miR-224 inhibit API-5 expression at the posttranscriptional level by degrading API-5 transcript resulting in reduced steady-state API-5 transcript levels (Fig. 3E).}
{Real-time polymerase chain reaction with reverse transcription (RT-PCR) analysis revealed a 1.960.2-fold increase in Mef2c mRNA levels in mutant granulocyte-monocyte progenitors (Fig. 3c). As a control for the specificity of Mef2c dysregulation in granulocyte-monocyte progenitors, we also evaluated the levels of this transcript in B cells (which do not express miR-223), where we observed unchanged Mef2c expression (Fig. 3c).}
{Real-time polymerase chain reaction with reverse transcription (RT-PCR) analysis revealed a 1.960.2-fold increase in Mef2c mRNA levels in mutant granulocyte-monocyte progenitors (Fig. 3c). As a control for the specificity of Mef2c dysregulation in granulocyte-monocyte progenitors, we also evaluated the levels of this transcript in B cells (which do not express miR-223), where we observed unchanged Mef2c expression (Fig. 3c).}
{To determine whether miR- 26a acts on Ezh2 at the mRNA level, miR-26a was transiently transfected into C2C12 myoblasts, and endogenous Ezh2 mRNA and protein expression was measured 48 h after transfection. In the presence of miR-26a, Ezh2 mRNA levels decreased significantly by 1.6-fold when compared with the control (Fig. 4e), and Ezh2 protein levels decreased by 1.5-fold (Fig. 4f). This result indicates that miR-26a is able to decrease Ezh2 mRNA levels.}
{By contrast, we did see significant up-regulation of GYS1 in Huh7 cells using LNA/OMe ON transfection (Fig. 3A), which agrees with data seen in mice for a MOE ON (Esau et al. 2006).}{We showed that three mRNAs, CAT-1, GYS1, and Aldolase A, are targets in Huh7 cells and three mRNAs, CAT-1, Aldolase A, and GTF2b, are targets in rat hepatocytes (Fig. 1). The amino acid transporter CAT-1 mRNA was shown by OMe ON inhibitor transfection to be a miR-122 target in Huh7 cells a few years ago (Chang et al. 2004), but another similar study also in Huh7 cells did not observe significant upregulation of CAT-1 mRNA levels by Northern blot analysis, but concluded instead that the mRNA was released from cytoplasmic processing P-bodies and recruited into polysomes (Bhattacharyya et al. 2006a,b).}
{To confirm this hypothesis, we transfected Huh7 cells and primary rat hepatocytes with LNA/OMe mixmers at different concentrations and measured in each case the levels of one of the down-regulated mRNAs (GYS1 and GTF2b, respectively).The results (Fig. 3) show that in both cell lines there is a dose-dependent increase in the intracellular concentration of the regulated mRNA obtained as the amount of transfected LNA/OMe ON is increased, but not for scrambled LNA/OMe ON (Fig. 3A,B). }
{We showed that three mRNAs, CAT-1, GYS1, and Aldolase A, are targets in Huh7 cells and three mRNAs, CAT-1, Aldolase A, and GTF2b, are targets in rat hepatocytes (Fig. 1). The amino acid transporter CAT-1 mRNA was shown by OMe ON inhibitor transfection to be a miR-122 target in Huh7 cells a few years ago (Chang et al. 2004), but another similar study also in Huh7 cells did not observe significant upregulation of CAT-1 mRNA levels by Northern blot analysis, but concluded instead that the mRNA was released from cytoplasmic processing P-bodies and recruited into polysomes (Bhattacharyya et al. 2006a,b).}
{We showed that three mRNAs, CAT-1, GYS1, and Aldolase A, are targets in Huh7 cells and three mRNAs, CAT-1, Aldolase A, and GTF2b, are targets in rat hepatocytes (Fig. 1). The amino acid transporter CAT-1 mRNA was shown by OMe ON inhibitor transfection to be a miR-122 target in Huh7 cells a few years ago (Chang et al. 2004), but another similar study also in Huh7 cells did not observe significant upregulation of CAT-1 mRNA levels by Northern blot analysis, but concluded instead that the mRNA was released from cytoplasmic processing P-bodies and recruited into polysomes (Bhattacharyya et al. 2006a,b).}
{We showed that three mRNAs, CAT-1, GYS1, and Aldolase A, are targets in Huh7 cells and three mRNAs, CAT-1, Aldolase A, and GTF2b, are targets in rat hepatocytes (Fig. 1). The amino acid transporter CAT-1 mRNA was shown by OMe ON inhibitor transfection to be a miR-122 target in Huh7 cells a few years ago (Chang et al. 2004), but another similar study also in Huh7 cells did not observe significant upregulation of CAT-1 mRNA levels by Northern blot analysis, but concluded instead that the mRNA was released from cytoplasmic processing P-bodies and recruited into polysomes (Bhattacharyya et al. 2006a,b).}
{We showed that three mRNAs, CAT-1, GYS1, and Aldolase A, are targets in Huh7 cells and three mRNAs, CAT-1, Aldolase A, and GTF2b, are targets in rat hepatocytes (Fig. 1). The amino acid transporter CAT-1 mRNA was shown by OMe ON inhibitor transfection to be a miR-122 target in Huh7 cells a few years ago (Chang et al. 2004), but another similar study also in Huh7 cells did not observe significant upregulation of CAT-1 mRNA levels by Northern blot analysis, but concluded instead that the mRNA was released from cytoplasmic processing P-bodies and recruited into polysomes (Bhattacharyya et al. 2006a,b).}
{We showed that three mRNAs, CAT-1, GYS1, and Aldolase A, are targets in Huh7 cells and three mRNAs, CAT-1, Aldolase A, and GTF2b, are targets in rat hepatocytes (Fig. 1). The amino acid transporter CAT-1 mRNA was shown by OMe ON inhibitor transfection to be a miR-122 target in Huh7 cells a few years ago (Chang et al. 2004), but another similar study also in Huh7 cells did not observe significant upregulation of CAT-1 mRNA levels by Northern blot analysis, but concluded instead that the mRNA was released from cytoplasmic processing P-bodies and recruited into polysomes (Bhattacharyya et al. 2006a,b).}
{To corroborate this result, we generated a siRNA construct containing two hairpin structures complementary to Fus-1 sequences (SI Fig. 16A). Down-regulation of Fus-1 was confirmed by RT-PCR (SI Fig. 16B) and Western blot (SI Fig. 16C).}{Cotransfection of miR-378 with FusUTR produced lower levels of Fus-1 protein than cotransfection of GFP vector with FusUTR (Fig. 5D Upper). RT-PCR analysis ofmRNAfrom these cells produced similar levels of PCR products (Fig. 5D Lower), indicating that miR-378 only affected Fus-1 at the protein level.}
{RT-PCR analysis detected little difference (SI Fig. 10C), indicating that miR-378 repressed Sufu expression at the translational level.}
{To further investigate the mode of regulation of miR-196b, we designed two primer sets (Fig.6A), in which one primer set encompasses the miR-196 binding and cleavage sites, and the other primer set is located 35 nt upstream of the miR-196 binding site and will therefore amplify the polyadenylated 5_ segment of the cleaved Hoxb8a mRNA. Results show a significant decrease in Hoxb8a expression in whole-body homogenates after E2 treatment with the primer set that encompasses miR-196b cleavage site (Fig.6B), indicating that miR-196b repressed Hoxb8a expression. However, E2 treatment did not change the Hoxb8a expression in the skin, possibly due to the general low level of expression of Hoxb8a in this tissue (data not shown).}
{Moreover, AldoA protein levels were 3-fold increased in LNAantimiR- treated mice compared to saline control mice (Figure 3D), concurring with the observed 2-fold derepression of AldoA message levels in LNA-treated mice (Figure 3B).}
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{Ectopic expression of miR-101 precursor in EL4 cells reduced endogenous Icos mRNA levels (Fig. 4c).}
{MiR-103 and miR-338 are both also predicted to recognize MTR1; ectopic expression of the miR-103 precursor, but not the miR-338 precursor, also reduced endogenous Icos mRNA levels (Supplementary Fig. 11).}
{Interestingly, both VSNL1 and GRIA2 expression was suppressed by 67 and 41%, respectively, in response to elevated miR-181b in HEK293 cells and SH-SY5Y cells, respectively (Fig. 4).}
{Interestingly, both VSNL1 and GRIA2 expression was suppressed by 67 and 41%, respectively, in response to elevated miR-181b in HEK293 cells and SH-SY5Y cells, respectively (Fig. 4).}
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{We then showed that introduction of exogenous synthetic miR-126*-mimic in LNCaP cells silenced prostein protein expression, while the mRNA level remained unaffected (Fig. 3a).}
{We then showed that introduction of exogenous synthetic miR-126*-mimic in LNCaP cells silenced prostein protein expression, while the mRNA level remained unaffected (Fig. 3a).}
{The levels of Smad1 mRNA were not affected by the inhibition of miR-26a with antisense 2'-O-methyl RNA (Fig. 3B),}
{Immunoblotting and RT-PCR analyses revealed that PTEN protein but not mRNA was considerably decreased in miR-214-transfected HIOSE-80 cells (Fig. 2B).}
{We tested whether endogenous p21 mRNA and protein levels fluctuate upon miR-106b gain of function and knockdown. miR-106b reduced p21 mRNA levels by 38% (Fig. 4A) and p21 protein levels by 46%, as usually observed for microRNA-mediated target down-regulation (2).}
{The precursor miR-126 does not affect VCAM-1 mRNA expression (Fig. 3F).}
{we found that transfection of 2.3 _ 105 rat 1a-c-Myc cells with pre-let-7a resulted in an increase at 48 h posttransfection of let-7a miRNA and a concomitant decrease in Myc mRNA (Table 2).}
{By both QRT-PCR (Figure 4A) and Western blot (Figure 4B), miR-130a strongly down-regulated endogenous GAX expression.}{Finally, cotransfecting with a 2'-O-methyl-modified oligo-RNA miR-130a inhibitor more than reversed the underexpression of endogenous GAX expression attributable to serum (Figure 4E).We conclude from these experiments that miR-130a regulates GAX expression through its consensus sequences in the 3'-UTR of the GAX gene.}
{Next, we determined whether transfection of cell lines with pre-miR-21, or anti-miR-21, affects Pdcd4 protein expression and invasion. In RKO colon cancer cells characterized by a high miR-21 expression, underexpression of endogenous miR-21 with anti-miR-21 (Figure 4a) led to a significant increase in Pdcd4 protein (Figure 4c) without any change in Pdcd4-mRNA (Figure 4b).}{Whereas Pdcd4 mRNA was almost unaltered in pre-miR-21-transfected cells (Figure 4f), there was a significant reduction of Pdcd4 protein amounts in pre-miR-21-transfected cells (Figure 4g),}
{At 3 months, RT-PCR, realtime PCR and western blot analysis of the clone cells demonstrated decreased PRDX6 expression compared with parental cells (P < 0.05; Additional file 2).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{All 18 genes showed, to varying degrees, increased mRNA expression levels upon miR-21 inhibition (Fig. 2B).}{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{Following normalization and statistical analysis we found 737 transcripts with significantly different expression between the LNA-miR-21-transfected cells and the controls, of which 402 (55%) were up-regulated and 335 (45%) down-regulated upon miR-21 inhibition (Fig. 2A and supplemental Table S1).}
{No change was seen in MeCP2 mRNA levels (Supplementary Fig. 10 online) or the protein levels of CtBP (Supplementary Fig. 9), a miR132 target whose MRE differs from the one in MeCP2, demonstrating specificity.}
{After confirming the expression of mature miR-218 (Figure 4a), we found that only the LAMB3 transcript was significantly underexpressed in miR-218-expressing cells (Figure 4b; data not shown)}{After confirming the expression of mature miR-218 (Figure 4a), we found that only the LAMB3 transcript was significantly underexpressed in miR-218-expressing cells (Figure 4b; data not shown)}
{Indeed, using quantitative real-time PCR, we identified CDC25A underexpression and reconfirmed BCL7A underexpression in the let-7b transfected WERI-Rb1 cells (Fig. 3b,c).}
{Indeed, using quantitative real-time PCR, we identified CDC25A underexpression and reconfirmed BCL7A underexpression in the let-7b transfected WERI-Rb1 cells (Fig. 3b,c).}
{We further validated the expression of five other genes upregulated in miR155-deficient B cells that contain miR-155 binding sites in their 30UTRs, by quantitative PCR (Figure 7A).}
{We further validated the expression of five other genes upregulated in miR155-deficient B cells that contain miR-155 binding sites in their 30UTRs, by quantitative PCR (Figure 7A).}
{We further validated the expression of five other genes upregulated in miR155-deficient B cells that contain miR-155 binding sites in their 30UTRs, by quantitative PCR (Figure 7A).}
{We further validated the expression of five other genes upregulated in miR155-deficient B cells that contain miR-155 binding sites in their 30UTRs, by quantitative PCR (Figure 7A).}
{We further validated the expression of five other genes upregulated in miR155-deficient B cells that contain miR-155 binding sites in their 30UTRs, by quantitative PCR (Figure 7A).}
{We therefore evaluated the effect of miR-125b on the expression of this gene. RT-PCR analysis of RNA extracted from miR-125bm-treated LNCaP cells exhibited a marked decrease in the expression of BAK1 (Fig. 6A), thus validating the microarray results.}{Next, we examined the level of Bak1 protein in miR-125bm- and antimiR-125b-treated LNCaP and/or cds1 cells. Transfection with miR-125bm led to _70% down-regulation of Bak1 in both cell lines (Fig. 6B), whereas treatment with anti-miR-125b induced 200% increase in the Bak1 in LNCaP cells (Fig. 6C).}{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{The results (by TaqMan real-time RT-PCR) of repeated experiments are summarized in Fig. 5. As expected, siRNA markedly decreases IRS-1 levels, but these remain constant in cells transfected with miR145 synthetic oligos. In fact, there was a small increase of IRS-1 mRNA in cells transfected with the miR oligo. The increase at 96 h was actually statistically significant. These experiments show that miR145 down-regulates the IRS-1 protein, but not the mRNA.}
{The results (by TaqMan real-time RT-PCR) of repeated experiments are summarized in Fig. 5. As expected, siRNA markedly decreases IRS-1 levels, but these remain constant in cells transfected with miR145 synthetic oligos. In fact, there was a small increase of IRS-1 mRNA in cells transfected with the miR oligo. The increase at 96 h was actually statistically significant. These experiments show that miR145 down-regulates the IRS-1 protein, but not the mRNA.}
{We have monitored c-MYC expression at the mRNA and protein levels following the inhibition of let-7 with the antisense synthetic let-7 oligo (anti-let-7c from Dharmacon) in HeLa cells. 48 h post-transfection RNAs and proteins were extracted from HeLa cells and analysed by Northern and Western methods, respectively. We detected a mild increase at the mRNA level and quite a significant increase at the protein level (Fig. 4A and 4B).}
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{Upon Pre-miR-134 treatment, LRH1, G_o, and Nanog mRNA levels did not change, and FADD mRNA levels increased.}
{Upon Pre-miR-134 treatment, LRH1, G_o, and Nanog mRNA levels did not change, and FADD mRNA levels increased.}
{Upon Pre-miR-134 treatment, LRH1, G_o, and Nanog mRNA levels did not change, and FADD mRNA levels increased.}
{We first verified the microarray results by quantitative real-time RT-PCR. atrophin mRNA levels were _2-fold higher in homozygous miR-8 mutants at early pupal stages (Figure 4A).}
{We first verified the microarray results by quantitative real-time RT-PCR. atrophin mRNA levels were _2-fold higher in homozygous miR-8 mutants at early pupal stages (Figure 4A).}
{We first verified the microarray results by quantitative real-time RT-PCR. atrophin mRNA levels were _2-fold higher in homozygous miR-8 mutants at early pupal stages (Figure 4A).}
{We first verified the microarray results by quantitative real-time RT-PCR. atrophin mRNA levels were _2-fold higher in homozygous miR-8 mutants at early pupal stages (Figure 4A).}
{To determine whether miR-322 regulates galectin-3 expression, BT549/vector cells were transfected with an antisense 2'-O-methyl oligoribonucleotide targeted against miR-322 or, as a control,with a scrambled 2'-O-methyl oligoribonucleotide. We found that anti-miR-322, and not the scrambled oligo, upregulates galectin-3 expression at the mRNA(Figure S3A, left) and protein levels (Figure S3A, right).}
{However, the repression on TRIM71 reporter was clearly demonstrated to an even greater extent than transfection with 2 nM oligo(pre-let7/pre-ctrl: 8.7 vs. 12.7%) (fig. 1D). These results confirm that the 3# UTR of TRIM71 contains the putative target sites for let-7a, whereas let-7a has little or no effect on the 3# UTRs of VDR, NR1I2, and FOXA1.}
{However, the repression on TRIM71 reporter was clearly demonstrated to an even greater extent than transfection with 2 nM oligo(pre-let7/pre-ctrl: 8.7 vs. 12.7%) (fig. 1D). These results confirm that the 3# UTR of TRIM71 contains the putative target sites for let-7a, whereas let-7a has little or no effect on the 3# UTRs of VDR, NR1I2, and FOXA1.}
{As shown in figure 2C, let-7c effectively repressed TRIM71 reporter as did let-7a (pre-let7/pre-ctrl: 11.5% of let-7c vs. 12.7% of let-7a). Besides, let-7c greatly repressed plet7AS control reporter, too, even though there is a nucleotide mismatch between them. These results suggest that TRIM71 is regulated not only by hsa-let-7a but also by other members of the human let-7 family.}
{The result showed that let-7a repressed the DLIN41 reporter to a similar extent as the TRIM71 reporter (pre-let7/pre-ctrl: 14.2% vs. 12.7%) (fig. 3B), suggesting that both TRIM71 and zebrafish lin-41 are evolutionarily conserved targets of let-7.}
{The result showed that let-7a repressed the DLIN41 reporter to a similar extent as the TRIM71 reporter (pre-let7/pre-ctrl: 14.2% vs. 12.7%) (fig. 3B), suggesting that both TRIM71 and zebrafish lin-41 are evolutionarily conserved targets of let-7.}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}{Overexpression of individual miR-29s induced marked reduction of DNMT3A and -3B mRNA levels. On the other hand, silencing of miR-29s with antisense molecules induced up-regulation of DNMT3A and -3B mRNA levels (Fig. 3b, Lower).}
{We observed that ectopic expression of miR-24 led to a 50% decrease of the hALK4 mRNA level in HEK293 cells (Figure 2A). Consistently, the endogenous hALK4 protein level was also apparently reduced by miR-24 (Figure 2B).}
{We observed that ectopic expression of miR-24 led to a 50% decrease of the hALK4 mRNA level in HEK293 cells (Figure 2A). Consistently, the endogenous hALK4 protein level was also apparently reduced by miR-24 (Figure 2B).}
{The levels of Smad1 mRNA were not affected by the inhibition of miR-26a with antisense 2_-O-methyl RNA (Fig. 3B), even though the protein levels increased, supporting a posttranscriptional mechanism of action.}
{In HeLa cells, eight potential mir-29c target mRNAs were detected at higher than background levels, and five of these were reduced significantly by mir-29c transfection: collagen 3A1, 4A1, 15A1, laminin1, and thymine-DNA glycosylase (TDG) (Fig. 1).}
{In HeLa cells, eight potential mir-29c target mRNAs were detected at higher than background levels, and five of these were reduced significantly by mir-29c transfection: collagen 3A1, 4A1, 15A1, laminin1, and thymine-DNA glycosylase (TDG) (Fig. 1).}
{In HeLa cells, eight potential mir-29c target mRNAs were detected at higher than background levels, and five of these were reduced significantly by mir-29c transfection: collagen 3A1, 4A1, 15A1, laminin1, and thymine-DNA glycosylase (TDG) (Fig. 1).}
{In HeLa cells, eight potential mir-29c target mRNAs were detected at higher than background levels, and five of these were reduced significantly by mir-29c transfection: collagen 3A1, 4A1, 15A1, laminin1, and thymine-DNA glycosylase (TDG) (Fig. 1).}
{In HeLa cells, eight potential mir-29c target mRNAs were detected at higher than background levels, and five of these were reduced significantly by mir-29c transfection: collagen 3A1, 4A1, 15A1, laminin1, and thymine-DNA glycosylase (TDG) (Fig. 1).}
{In HeLa cells, eight potential mir-29c target mRNAs were detected at higher than background levels, and five of these were reduced significantly by mir-29c transfection: collagen 3A1, 4A1, 15A1, laminin1, and thymine-DNA glycosylase (TDG) (Fig. 1).}
{In HeLa cells, eight potential mir-29c target mRNAs were detected at higher than background levels, and five of these were reduced significantly by mir-29c transfection: collagen 3A1, 4A1, 15A1, laminin1, and thymine-DNA glycosylase (TDG) (Fig. 1).}
{In addition, HepG2 cells showed mir-29c-mediated reductions for two additional candidate, target genes, fibrillin 1, and FUSIP1 (Fig. 1).}
{In addition, HepG2 cells showed mir-29c-mediated reductions for two additional candidate, target genes, fibrillin 1, and FUSIP1 (Fig. 1).}
{A dramatic increase in E-cadherin expression was accompanied by a significant decrease in ZEB1 and ZEB2 mRNA levels (Fig. 2F).}
{A dramatic increase in E-cadherin expression was accompanied by a significant decrease in ZEB1 and ZEB2 mRNA levels (Fig. 2F).}
{A dramatic increase in E-cadherin expression was accompanied by a significant decrease in ZEB1 and ZEB2 mRNA levels (Fig. 2F).}
{A dramatic increase in E-cadherin expression was accompanied by a significant decrease in ZEB1 and ZEB2 mRNA levels (Fig. 2F).}
{A dramatic increase in E-cadherin expression was accompanied by a significant decrease in ZEB1 and ZEB2 mRNA levels (Fig. 2F).}
{A dramatic increase in E-cadherin expression was accompanied by a significant decrease in ZEB1 and ZEB2 mRNA levels (Fig. 2F).}
{A dramatic increase in E-cadherin expression was accompanied by a significant decrease in ZEB1 and ZEB2 mRNA levels (Fig. 2F).}
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{[accessed from the pictures]}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{Transfection of let-7 duplex to H1299 reduced the HMGA2 mRNA and protein(Fig. 2B; Supplementary Fig. S2D).}{Inhibition of let-7 in HeLa cells induced HMGA2 mRNA and protein (Fig. 2C).}
{In concordance with the microarray results, a significant induction of c-Maf mRNAwas detected in bicm2/m2 Th2 cells, and the levels of c-Maf protein were correspondingly increased (Fig. 4,C and D).}
{Increasing let-7C expression in Hepa-1 cells (Fig.3C) decreased c-myc gene expression in a dose-dependent manner (Fig. 3D).}
{We showed that delivering miR-124a2 causes no significant change in Foxa2 mRNA expression, whereas the anti-miR-124a2 induced more than a 2-fold increase in the Foxa2 transcript (Fig. 2C)}{We showed that delivering miR-124a2 causes no significant change in Foxa2 mRNA expression, whereas the anti-miR-124a2 induced more than a 2-fold increase in the Foxa2 transcript (Fig. 2C)}
{On the other hand, the level of ERK5 mRNAs evaluated by qRT-PCR in DLD-1 cells was almost unchanged in the same samples (Fig. 6C), which indicated that the introduction of exogenous miR-143 precursor miRNAs caused the decreased expression of the ERK5 protein at the translational level.}
{Also, in agreement with recent reports of mRNA degradation associated with miRNA-mediated regulation (2), we observed some (_35%) degradation of our LCS-containing reporter mRNAs relative to their reversed,mutated LCS controls (determined by RNase protection) (Fig.1 D and E).}
{Fig. 2A shows that LNCaP cells transduced with p-221, p-222, or p-T clearly expressed high levels of the expected mature microRNAs, whereas very little expression was detected in control-transduced cells.}
{Fig. 2A shows that LNCaP cells transduced with p-221, p-222, or p-T clearly expressed high levels of the expected mature microRNAs, whereas very little expression was detected in control-transduced cells.}
{Fig. 2A shows that LNCaP cells transduced with p-221, p-222, or p-T clearly expressed high levels of the expected mature microRNAs, whereas very little expression was detected in control-transduced cells.}
{Fig. 2A shows that LNCaP cells transduced with p-221, p-222, or p-T clearly expressed high levels of the expected mature microRNAs, whereas very little expression was detected in control-transduced cells.}
{Fig. 2A shows that LNCaP cells transduced with p-221, p-222, or p-T clearly expressed high levels of the expected mature microRNAs, whereas very little expression was detected in control-transduced cells.}
{Fig. 2A shows that LNCaP cells transduced with p-221, p-222, or p-T clearly expressed high levels of the expected mature microRNAs, whereas very little expression was detected in control-transduced cells.}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{HMGA2 expression was substantially reduced on introduction of the let-7 miRNAs (Fig. 2B). Introduction of exogenous let-7a, let-7c, or let-7g caused degradation of HMGA2 mRNA (Fig. 2C).}
{As evident from Figure 3D,E, miR-200b markedly reduced ZFHX1B protein and mRNA levels compared to mock transfected cells. In contrast, none of the control miRNAs repressed ZFHX1B.}{As evident from Figure 3D,E, miR-200b markedly reduced ZFHX1B protein and mRNA levels compared to mock transfected cells. In contrast, none of the control miRNAs repressed ZFHX1B.}
{To investigate whether transfection of miR-155 and/or mutant miR-155 resulted in the degradation of hAT1R mRNAs, real time PCR experiments were performed. The results of these experiments demonstrated that these miRNAs did not decrease hAT1R protein levels by mediating increasedmRNAdegradation (Fig. 4, D and E).}{To investigate whether transfection of miR-155 and/or mutant miR-155 resulted in the degradation of hAT1R mRNAs, real time PCR experiments were performed. The results of these experiments demonstrated that these miRNAs did not decrease hAT1R protein levels by mediating increasedmRNAdegradation (Fig. 4, D and E).}
{Consistent with the hypothesis that AML1 translation is negatively regulated by miRNA 17-5p-20a-106a, a 50-60% reduction in AML1 protein level was observed in cells transfected with these miRNAs compared to those transfected with scrambled control oligonucleotides (see Supplementary Information,Fig. S3a) and conversely, no fluctuation in AML1 mRNA levels was observed (see Supplementary Information, Fig. S3b).}{When antimiRNAs were transfected, the level of endogenous miRNAs 17-5p, 20a and 106a declined (see Supplementary Information, Fig. S2b) coupled with increased expression of AML1 protein, whereas the mRNA abundance was unaffected (see Supplementary Information, Fig. S3c, d).}
{Consistent with the hypothesis that AML1 translation is negatively regulated by miRNA 17-5p-20a-106a, a 50-60% reduction in AML1 protein level was observed in cells transfected with these miRNAs compared to those transfected with scrambled control oligonucleotides (see Supplementary Information,Fig. S3a) and conversely, no fluctuation in AML1 mRNA levels was observed (see Supplementary Information, Fig. S3b).}{When antimiRNAs were transfected, the level of endogenous miRNAs 17-5p, 20a and 106a declined (see Supplementary Information, Fig. S2b) coupled with increased expression of AML1 protein, whereas the mRNA abundance was unaffected (see Supplementary Information, Fig. S3c, d).}
{Consistent with the hypothesis that AML1 translation is negatively regulated by miRNA 17-5p-20a-106a, a 50-60% reduction in AML1 protein level was observed in cells transfected with these miRNAs compared to those transfected with scrambled control oligonucleotides (see Supplementary Information,Fig. S3a) and conversely, no fluctuation in AML1 mRNA levels was observed (see Supplementary Information, Fig. S3b).}{When antimiRNAs were transfected, the level of endogenous miRNAs 17-5p, 20a and 106a declined (see Supplementary Information, Fig. S2b) coupled with increased expression of AML1 protein, whereas the mRNA abundance was unaffected (see Supplementary Information, Fig. S3c, d).}
{Intriguingly, by quantitative RT-PCR, we found that the mRNA level of p27 remained unaltered in the miR-221-transduced cells, indicating that miR-221 controls p27Kip1 translation but not mRNA stability (Figure 2E).}
{To test whether let-7i can induce cleavage of TLR4 mRNA, we measured the mRNA level of TLR4 in cultured cholangiocytes transfected with either let-7i antisense 2-methoxy oligonucleotides or let-7i precursor by quantitative RT-PCR. No significant difference of TLR4 mRNA was found in cells transfected with either let-7i antisense 2-methoxy oligonucleotides or let-7i precursor (Fig. 3A).}{To test whether let-7i can induce cleavage of TLR4 mRNA, we measured the mRNA level of TLR4 in cultured cholangiocytes transfected with either let-7i antisense 2-methoxy oligonucleotides or let-7i precursor by quantitative RT-PCR. No significant difference of TLR4 mRNA was found in cells transfected with either let-7i antisense 2-methoxy oligonucleotides or let-7i precursor (Fig. 3A).}
{Western Blot demonstrated decreased Bcl-2 protein level in miR-15b or miR-16 precursor-transfected cells compared to precursor control-transfected cells. In contrast, RT-PCR did not show any difference in the mRNA level (Fig. 3c).}
{Western Blot demonstrated decreased Bcl-2 protein level in miR-15b or miR-16 precursor-transfected cells compared to precursor control-transfected cells. In contrast, RT-PCR did not show any difference in the mRNA level (Fig. 3c).}
{Similar results were found with miR-155-deficient B cells, which show a 2.5-fold increase in Aicda mRNA after 4 days (Figure 1F).}{Consistent with elevated amounts of AID protein, the corresponding mRNA was elevated in Aicda155/_ when compared to Aicda+/_ controls beginning 2 days after stimulation with LPS and IL-4 (Figure 1E).}
{On the other hand, AMO-1 and AMO-133,transfected alone or together, failed to produce any significant effects on HCN2 and HCN4 mRNA levels (Fig. 2F and 2G), indicating that the miRNAs do not affect HCN2/HCN4 mRNA stability.}
{On the other hand, AMO-1 and AMO-133,transfected alone or together, failed to produce any significant effects on HCN2 and HCN4 mRNA levels (Fig. 2F and 2G), indicating that the miRNAs do not affect HCN2/HCN4 mRNA stability.}
{On the other hand, AMO-1 and AMO-133,transfected alone or together, failed to produce any significant effects on HCN2 and HCN4 mRNA levels (Fig. 2F and 2G), indicating that the miRNAs do not affect HCN2/HCN4 mRNA stability.}
{Consistent with translational inhibition by microRNAs, we notedd ecreasedEGFR protein andnot mRNA (real-time PCR data not shown).}
{Consistent with translational inhibition by microRNAs, we notedd ecreasedEGFR protein andnot mRNA (real-time PCR data not shown).}
{Consistent with translational inhibition by microRNAs, we notedd ecreasedEGFR protein andnot mRNA (real-time PCR data not shown).}
{On the contrary, treatment of differentiated cancer cell lines HPAF2 and MCF7 with inhibitors of miR-200c or miR-141 resulted in a change in the expression of characteristic genes, including an increase in ZEB1 and TGFb2 expression (supplementary Fig 3C online).}
{On the contrary, treatment of differentiated cancer cell lines HPAF2 and MCF7 with inhibitors of miR-200c or miR-141 resulted in a change in the expression of characteristic genes, including an increase in ZEB1 and TGFb2 expression (supplementary Fig 3C online).}
{On the contrary, treatment of differentiated cancer cell lines HPAF2 and MCF7 with inhibitors of miR-200c or miR-141 resulted in a change in the expression of characteristic genes, including an increase in ZEB1 and TGFb2 expression (supplementary Fig 3C online).}
{The sequence of the target site can not match the sequence of the targe gene stored in NCBI.}
{The sequence of the target site can not match the sequence of the targe gene stored in NCBI.}
{The sequence of the target site can not match the sequence of the targe gene stored in NCBI.}
{The increased levels of miRNA-98 were validated by miRVana qRT-PCRô as before. These treatments resulted in diminishment in protein levels and mRNA expression of HMGA2 in control the normoxic SCC-4 cell line as well as cell lines exposed to hypoxia (Figure 9a,b);}{Anti-miR98ô transfection had a significant effect on enhancing HMGA2 expression when cells lines were grown during normoxia (*p ? 0.05) but were ineffective under hypoxic conditions.}
{The increased levels of miRNA-98 were validated by miRVana qRT-PCRô as before. These treatments resulted in diminishment in protein levels and mRNA expression of HMGA2 in control the normoxic SCC-4 cell line as well as cell lines exposed to hypoxia (Figure 9a,b);}{Anti-miR98ô transfection had a significant effect on enhancing HMGA2 expression when cells lines were grown during normoxia (*p ? 0.05) but were ineffective under hypoxic conditions.}
{The increased levels of miRNA-98 were validated by miRVana qRT-PCRô as before. These treatments resulted in diminishment in protein levels and mRNA expression of HMGA2 in control the normoxic SCC-4 cell line as well as cell lines exposed to hypoxia (Figure 9a,b);}{Anti-miR98ô transfection had a significant effect on enhancing HMGA2 expression when cells lines were grown during normoxia (*p ? 0.05) but were ineffective under hypoxic conditions.}
{The increased levels of miRNA-98 were validated by miRVana qRT-PCRô as before. These treatments resulted in diminishment in protein levels and mRNA expression of HMGA2 in control the normoxic SCC-4 cell line as well as cell lines exposed to hypoxia (Figure 9a,b);}{Anti-miR98ô transfection had a significant effect on enhancing HMGA2 expression when cells lines were grown during normoxia (*p ? 0.05) but were ineffective under hypoxic conditions.}
{The increased levels of miRNA-98 were validated by miRVana qRT-PCRô as before. These treatments resulted in diminishment in protein levels and mRNA expression of HMGA2 in control the normoxic SCC-4 cell line as well as cell lines exposed to hypoxia (Figure 9a,b);}{Anti-miR98ô transfection had a significant effect on enhancing HMGA2 expression when cells lines were grown during normoxia (*p ? 0.05) but were ineffective under hypoxic conditions.}
{The increased levels of miRNA-98 were validated by miRVana qRT-PCRô as before. These treatments resulted in diminishment in protein levels and mRNA expression of HMGA2 in control the normoxic SCC-4 cell line as well as cell lines exposed to hypoxia (Figure 9a,b);}{Anti-miR98ô transfection had a significant effect on enhancing HMGA2 expression when cells lines were grown during normoxia (*p ? 0.05) but were ineffective under hypoxic conditions.}
{The increased levels of miRNA-98 were validated by miRVana qRT-PCRô as before. These treatments resulted in diminishment in protein levels and mRNA expression of HMGA2 in control the normoxic SCC-4 cell line as well as cell lines exposed to hypoxia (Figure 9a,b);}{Anti-miR98ô transfection had a significant effect on enhancing HMGA2 expression when cells lines were grown during normoxia (*p ? 0.05) but were ineffective under hypoxic conditions.}
{Transfection with various concentrations of premiR-206, a synthetic RNA duplex that mimics endogenousmiR-206, induces a dose- and time-dependent repression of ER_ mRNA levels (Fig. 2A; and Fig. S1 published as supplemental data on The Endocrine Society's Journals Online web site at http://mend. endojournals.org).}{To further validate these results, MCF-7 cells were treated with 2_-O-methyl antagomiRs, which are single-stranded modified RNAs that have a complimentary sequence to mature miRNAs and function by sequestering/degrading endogenous miRNAs (51, 52). When 20 nM antagomiR-206 was transfected into MCF-7 cells, ER_ mRNA increased as much as 7.5-fold (Fig. 2B).}
{Transfection with various concentrations of premiR-206, a synthetic RNA duplex that mimics endogenousmiR-206, induces a dose- and time-dependent repression of ER_ mRNA levels (Fig. 2A; and Fig. S1 published as supplemental data on The Endocrine Society's Journals Online web site at http://mend. endojournals.org).}{To further validate these results, MCF-7 cells were treated with 2_-O-methyl antagomiRs, which are single-stranded modified RNAs that have a complimentary sequence to mature miRNAs and function by sequestering/degrading endogenous miRNAs (51, 52). When 20 nM antagomiR-206 was transfected into MCF-7 cells, ER_ mRNA increased as much as 7.5-fold (Fig. 2B).}
{Although miR-125b directed cleavage within the RNA element to which it was perfectly complementary, no such cleavage could be detected in or near the imperfectly complementary miRE1 element, which nonetheless mediated significant reductions in luciferase mRNA and protein levels (Fig. 1C and other data not shown; see also Fig. 7, which is published as supporting information on the PNAS web site).}
{Although miR-125b directed cleavage within the RNA element to which it was perfectly complementary, no such cleavage could be detected in or near the imperfectly complementary miRE1 element, which nonetheless mediated significant reductions in luciferase mRNA and protein levels (Fig. 1C and other data not shown; see also Fig. 7, which is published as supporting information on the PNAS web site).}
{In combination, L7 and let-7 proved to be as effective as miRE1 and miR-125b at repressing protein synthesis (15), as judged from the 89% decrease in expression of an L7-containing luciferase reporter (Luc_6L7) in the presence of let-7a. Furthermore, down-regulation of protein synthesis was accompanied by a smaller yet substantial decline in mRNA concentration (Fig. 3B).}
{As results, the level of HOXB8 in cells that expressed miR-196 was decreased compared with that in cells that expressed mutant miR-196. In addition, the level of HOXB8 mRNA was also decreased in the presence of exogenous miRNA. These results suggest that miR-196 can regulate expression of HOXB8 at a post-transcriptional level.}{As results, the level of HOXB8 in cells that expressed miR-196 was decreased compared with that in cells that expressed mutant miR-196. In addition, the level of HOXB8 mRNA was also decreased in the presence of exogenous miRNA. These results suggest that miR-196 can regulate expression of HOXB8 at a post-transcriptional level.}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{To validate the results obtained by transcriptomic or proteomic analyses, we assayed the expression of nine genes (four identified by the EST microarray, two by proteomics, and three identified by neither of the techniques and therefore considered as negative controls), by qRT-PCR in MEG-01 cells transfected with pRS15/16 or pRS-E (control). As shown in Fig. 2A, the transfection with miR-15a/16-1 reduces the expression of both microarray identified mRNAs (PDCD4, RAB21, IGSF4, SCAP2) and proteomics identified proteins (Bcl2, Wt1).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
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{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{The genes (mRNAs) with the highest-ranking scores for each database were selected as targets for the miRNA identified in our profiling analysis. The miRNA targets that were found in our DNA microarray analysis are listed in the Table.}
{No changes were detected inmRNA levels in Ad-375-infected cells compared to controls, indicating that the regulation of target gene expression by miR-375 is mainly posttranscriptional (Fig. 4c, d).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{By using a 2.0-fold difference as the cut-off, there were 60 differentially expressed genes: 13 were up-regulated and 47 were down-regulated (SI Tables 1 and 2).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{We selected genes that were low in miR-15/16 high-expressor CLLs and high in miR-15/16 low-expressor CLLs, which were intersected with genes down-regulated in MEG-01 cells after transfection with pRS15/16. A signature of 60 genes (70 probes) emerged (Table 4 and SI Table 11).}
{miR-1 or miR-124 RNA duplexes were transfected into HeLa cells, and mRNA was purified and profiled on microarrays (Fig. 1a). Filtering the expression profiles for genes characterized by the LocusLink database12 that were significantly downregulated (P , 0.001) at both 12 and 24 h, gave sets of 96 and 174 annotated genes downregulated by miR-1 and miR-124, respectively (Supplementary Tables 1 and 2).}
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{We selected Cdc34, a let-7 target that was strongly down-regulated with pre-let-7b transfection in our microarray experiments (Figure 2A)}
{Similar results were obtained using the other two miRNAs as the introduced silent mutations rescued the corresponding Nanog-,Oct4- and Sox2-CDS constructs from downregulation by pre-miR-470 and pre-miR-134 (Fig. 2b, c).}
{We transfected mouse ESCs with precursor miRNA (pre-miRNA) oligomers (see Methods) separately for each miRNA and measured the effect on the predicted corresponding endogenous target using quantitative PCR and western blotting. Each miRNA had only a limited effect on the mRNA of the endogenous target but affected the corresponding protein more substantially (Fig. 1a).}
{We transfected mouse ESCs with precursor miRNA (pre-miRNA) oligomers (see Methods) separately for each miRNA and measured the effect on the predicted corresponding endogenous target using quantitative PCR and western blotting. Each miRNA had only a limited effect on the mRNA of the endogenous target but affected the corresponding protein more substantially (Fig. 1a).}
{We transfected mouse ESCs with precursor miRNA (pre-miRNA) oligomers (see Methods) separately for each miRNA and measured the effect on the predicted corresponding endogenous target using quantitative PCR and western blotting. Each miRNA had only a limited effect on the mRNA of the endogenous target but affected the corresponding protein more substantially (Fig. 1a).}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch 1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{As shown in Figure 4,Notch1 and HMGA2 were inhibited by all three miR-34a,b, c mimics, while miR-34b mimic inhibited Notch2 and 4, and miR-34c mimic inhibited Notch1-4.}
{We found a significant dose-dependent decrease in c-myc mRNA in cells transfected with hsa-mir-34b (Figure 5b);}
{Immunoblotting and RT-PCR analyses revealed that RhoA protein but not RhoA mRNA was considerably decreased in miR-155-transfected cells (Fig. 5B).}
{Immunoblotting and RT-PCR analyses revealed that RhoA protein but not RhoA mRNA was considerably decreased in miR-155-transfected cells (Fig. 5B).}
{Immunoblotting and RT-PCR analyses revealed that RhoA protein but not RhoA mRNA was considerably decreased in miR-155-transfected cells (Fig. 5B).}
{Transient transfection of increasing amounts of miR-221 and/or miR-222 in MCF-7 cells reduced ERŒ±expression in a dose-dependent manner (Fig. 2B). Furthermore,stably miR-221- and miR-222-transfected MCF-7 and T47D cells decreased the protein but not mRNA levels of ERŒ±(Fig. 2C).}
{Transient transfection of increasing amounts of miR-221 and/or miR-222 in MCF-7 cells reduced ERŒ±expression in a dose-dependent manner (Fig. 2B). Furthermore,stably miR-221- and miR-222-transfected MCF-7 and T47D cells decreased the protein but not mRNA levels of ERŒ±(Fig. 2C).}
{Expression of miR-133 down-regulated endogenous Runx2 protein (Fig. 3C),with no effect on mRNA levels(Fig. 3D)}
{we performed real-time RT-PCR and found a consistent decrease in AID levels in miR-181b ‚Äì transduced when compared with control-transduced primary B cells (32% reduction;P = 0.004; Fig. 2 C ).}
{we performed real-time RT-PCR and found a consistent decrease in AID levels in miR-181b ‚Äì transduced when compared with control-transduced primary B cells (32% reduction;P = 0.004; Fig. 2 C ).}
{our preliminary data have shown that transfection of miR-146a into THP-1 monocytes results in knockdown of TRAF6 and IRAK-1 expression and inflammatory cytokine production (Pauley KM and coworkers, unpublished data). To investigate this possibility further, we transfected siRNA targeting TRAF6 and/or IRAK-1 into THP-1 cells. The knockdown efficiency was determined by analyzing TRAF6 and IRAK-1 mRNA levels by qRTPCR,and at least 80% and 60% knockdown was achieved for TRAF6 and IRAK-1, respectively (Figure 5a). }
{our preliminary data have shown that transfection of miR-146a into THP-1 monocytes results in knockdown of TRAF6 and IRAK-1 expression and inflammatory cytokine production (Pauley KM and coworkers, unpublished data). To investigate this possibility further, we transfected siRNA targeting TRAF6 and/or IRAK-1 into THP-1 cells. The knockdown efficiency was determined by analyzing TRAF6 and IRAK-1 mRNA levels by qRTPCR,and at least 80% and 60% knockdown was achieved for TRAF6 and IRAK-1, respectively (Figure 5a). }
{On the other hand, the downregulation of procaspase-3 by transfection with let-7a precursor was not detected at the mRNA level (Fig. 2b).}
{Further evidence of Smo repression through miRNA activity was provided by the reduction of Smo mRNA and protein levels following overexpression of miR-125b, miR-326 and miR-324-5p in Daoy cells (Figure 2E and F).}
{Further evidence of Smo repression through miRNA activity was provided by the reduction of Smo mRNA and protein levels following overexpression of miR-125b, miR-326 and miR-324-5p in Daoy cells (Figure 2E and F).}
{Further evidence of Smo repression through miRNA activity was provided by the reduction of Smo mRNA and protein levels following overexpression of miR-125b, miR-326 and miR-324-5p in Daoy cells (Figure 2E and F).}
{In hESCs transfected with anti-miR-302, mature miR-302a levels were decreased due to the fact that the anti-miR inhibitors bind irreversibly to the miRNA, causing them to be unavailable both functionally and for the analysis (Fig. 7A). Under these conditions, the cyclin D1 protein level was increased, but there was no change in the cyclin D1 mRNA level.}
{Real-time RT-PCR analysis showed that the mRNA level of p27Kip1 was also reduced in these cell lines(Fig. 3B),}
{Real-time RT-PCR analysis showed that the mRNA level of p27Kip1 was also reduced in these cell lines(Fig. 3B),}
{qRT‚ÄìPCR analysis showed a moderate reduction of CCND1 mRNA in HepG2 ells overexpressing miR-16 or miR-424 (Figure 2E)}
{qRT‚ÄìPCR analysis showed a moderate reduction of CCND1 mRNA in HepG2 ells overexpressing miR-16 or miR-424 (Figure 2E)}
{qRT‚ÄìPCR analysis showed a moderate reduction of CCND1 mRNA in HepG2 ells overexpressing miR-16 or miR-424 (Figure 2E)}
{Interestingly, let-7 repressed not only the protein level of Dicer but also its mRNA level (Figure 3C and D),}
{Interestingly, let-7 repressed not only the protein level of Dicer but also its mRNA level (Figure 3C and D),}
{No signifi cant difference in cyclin D1 mRNA levels was observed between miR-17/20 ‚Äì transduced cells and control cells ( Fig. 4 A )}
{No signifi cant difference in cyclin D1 mRNA levels was observed between miR-17/20 ‚Äì transduced cells and control cells ( Fig. 4 A )}
{We quantified mRNA expression of potential miR-126 targets by qRT-PCR in HUVECs that had been transfected with antisense miR-126 MO or a miR-126 mimic (Figure 4C)}
{We quantified mRNA expression of potential miR-126 targets by qRT-PCR in HUVECs that had been transfected with antisense miR-126 MO or a miR-126 mimic (Figure 4C)}
{We quantified mRNA expression of potential miR-126 targets by qRT-PCR in HUVECs that had been transfected with antisense miR-126 MO or a miR-126 mimic (Figure 4C)}
{Infection of HUVEC cells with an adenovirus expressing miR-126 also repressed expression of Spred-1 mRNA by about 2-fold (Figure 6F).}
{Real-time qRT-PCR was performed at 24 h post-transfection. The mRNA expression levels of Bcl-w were reduced to 77%, 81%, and 42% in Hep3B,HepG2, and HeLa cells, respectively, when compared to the vector-only control (pSM-vector) (Fig. 3A)}
{We utilized RT-QPCR to determine if miRNA overexpression resulted in decreased APP mRNA levels. Overexpression of mir-106a or mir-520c had no effect on APP mRNA levels (Figure 2E)}
{We utilized RT-QPCR to determine if miRNA overexpression resulted in decreased APP mRNA levels. Overexpression of mir-106a or mir-520c had no effect on APP mRNA levels (Figure 2E)}
{As illustrated in figure 3B, transfection with pre-miR-150 led to a reduction of c-Myb mRNA to 73% of the pre-ctrl or pre-miR-198 transfections.}
{As illustrated in figure 3B, transfection with pre-miR-150 led to a reduction of c-Myb mRNA to 73% of the pre-ctrl or pre-miR-198 transfections.}
{As shown in Figure 3B, miR-126 substantially reduced p85Œ≤ protein (~3-fold) with no apparent degradation of the transcript, thereby indicating a translational repression of the p85b mRNA by miR-126.}
{As shown in Figure 4a, transfection of cancer cells with miR-196a mimics resulted in a reproducible decrease of ANXA1 mRNA by 60‚Äì65% in BIC-1, 30-35% in SEG-1, 30‚Äì35% in MDA-231 and 40‚Äì45% in HEC1B cells when compared to the respective controls that were transfected with a nonspecific negative control RNA.}
{ figure 3C, levels of mdr1 mRNA in the MCF-7/DOX cell transfected with miR451}
{In addition, Fig. 4D shows that miR-17-92 also down-regulates PTPRO mRNA expression.}
{No differences in the HTR3E mRNA levels (normalized to neomycin transferase mRNA levels) were detectable for any combination of transfected constructs (Supplementary Material, Fig. S1)}
{the human IGF2R steady state mRNA levels were quantitated by RTqPCR experiments.The data demonstrate that hsa-miR-657 does not signif¬≠i¬≠cantly reduce human IGF2R mRNA levels compared with N.C. and mock (Fig. 3A), indicating that hsa-miR-657 does not target human IGF2R mRNA for degradation.}
{Transfection with 50 and 100 nM of pre-miR 126 resulted in a 1000 to 5000-fold increase in miR-126 expression measured by RT-PCR and a decrease in Crk II protein while mRNA remained unchanged (Fig. 3A and B)}
{To validate miR-21 regulation of RECK and TIMP3, we first confirmed RECK and TIMP3 mRNA elevation in miR-21 knocked-down A172 cells by qRT-PCR (Fig. 4C).RECK mRNA level increased consistently 2-fold and TIMP3 mRNA about 1.6-fold in the cells transfected with anti-miR-21.}
{To validate miR-21 regulation of RECK and TIMP3, we first confirmed RECK and TIMP3 mRNA elevation in miR-21 knocked-down A172 cells by qRT-PCR (Fig. 4C).RECK mRNA level increased consistently 2-fold and TIMP3 mRNA about 1.6-fold in the cells transfected with anti-miR-21.}
{In independent experiments we observed marked reductions of CDK6 transcript (Figure 6A) and CDK6 protein (Figure 6B) in response to miR-124 and miR-137 transfection}
{In independent experiments we observed marked reductions of CDK6 transcript (Figure 6A) and CDK6 protein (Figure 6B) in response to miR-124 and miR-137 transfection}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR was performed on 8 genes found to be targets of let-7f(KIF1A, ASS, FDPS, NTS in UCI-101 cells, and TFF1, EEF1A2,ESM1, VIM, in BG-1 cells) (Figure 5)}
{RT-PCR assays showed little difference in the cells transfected with miR-328 as compared with the cells transfected with the control vector (Figure 3B, right panel)}
{Furthermore, overexpression of miR-221 or miR-222 by Ad-miR-221 or Ad-miR-222 decreased p27(Kip1) mRNA level but had no effect on p57(Kip2) mRNA level(Figure 4F)}
{Furthermore, overexpression of miR-221 or miR-222 by Ad-miR-221 or Ad-miR-222 decreased p27(Kip1) mRNA level but had no effect on p57(Kip2) mRNA level(Figure 4F)}
{Furthermore, overexpression of miR-221 or miR-222 by Ad-miR-221 or Ad-miR-222 decreased p27(Kip1) mRNA level but had no effect on p57(Kip2) mRNA level(Figure 4F)}
{Furthermore, overexpression of miR-221 or miR-222 by Ad-miR-221 or Ad-miR-222 decreased p27(Kip1) mRNA level but had no effect on p57(Kip2) mRNA level(Figure 4F)}
{Overexpression of miR106b was associated with a decrease in Itch protein levels (Figure 4E),but had no effect on Itch mRNA levels (Figure 4D)}
{We also analyzed the expression level of DHFR mRNA using real-time qRT-PCR analysis and the results (Fig. 1C) indicated that there was no reduction in DHFR mRNA expression by miR-192 (lane 4) and miR-24 (lane 5)}
{Similarly, KU812 cells nucleofected with pre-miR-10 showed an increase in expression of hsa-miR-10a and a decrease in HOXA1 mRNA and USF2 mRNA and protein levels (Fig.3A and B)}
{To confirm the Raf1 microarray result, we performed qRT-PCR on RNA from A549 cells transfected with miR-7 or miR-NC. This showed downregulation of the expression of Raf1 mRNA relative to GAPDH mRNA with miR-7 (Fig. 5A), suggesting thatmiR-7 promotes decay of Raf1 mRNA}
{To confirm the Raf1 microarray result, we performed qRT-PCR on RNA from A549 cells transfected with miR-7 or miR-NC. This showed downregulation of the expression of Raf1 mRNA relative to GAPDH mRNA with miR-7 (Fig. 5A), suggesting thatmiR-7 promotes decay of Raf1 mRNA}
{Compared to transfection with miR-NC precursor, transfection with miR-7 precursor reduced EGFR mRNA expression significantly in A549, U87, MDA-MB-468 and DU145 cells at 24 h posttransfection by qRT-PCR (Fig. 2A)}
{Compared to transfection with miR-NC precursor, transfection with miR-7 precursor reduced EGFR mRNA expression significantly in A549, U87, MDA-MB-468 and DU145 cells at 24 h posttransfection by qRT-PCR (Fig. 2A)}
{Western blot and real-time PCR analysis showed that HOXC8 expression was decreased in miR-196a-overexpressing hASC but increased in anti-miR-196a-transfected hASC(Fig 6C and D, respectively)}
{COX-2 mRNA levels were also evaluated and no significant modification was observed following the different treatments withthe exception of the transfection of siCOX-2 (Figs. 2B‚ÄìD)}
{we monitored COXIV mRNA levels after transfecting the soma or the distal axons with the miR-338 precursor (pre-miR-338). COXIV mRNA levels decreased ~80% in both neuronal compartments when compared with the nontargeting pre-miR-NT (Fig. 4A}
{we measured LMO2 mRNA and protein in pcDNA3.1-pri-miR-223/K562 cells by real-time PCR and Western blot analysis. LMO2 mRNA levels in pcDNA3.1-pri-miR-223/K562 cells were much lower than that in pcDNA3.1/K562 cells both before and after hemin induction (Fig.8B)}
{Quantitative reverse transcription polymerase chain reaction (RT-PCR) demonstrated a reduction in EZH2 transcript levels by miR-101 (Fig. 1C)}
{Quantitative reverse transcription polymerase chain reaction (RT-PCR) demonstrated a reduction in EZH2 transcript levels by miR-101 (Fig. 1C)}
{Furthermore, miR-138 RNA injection into zebrafish embryos decreased endogenous cspg2 mRNA levels by 90% (Fig. 5D)}
{Introduction of miR-138 into mouse NIH 3T3 cells decreased endogenous cspg2 mRNA and protein accumulation by approximately 40% (Fig. 5 B and C)}
{Injection of pri-miR-138 into fish decreased, and exposure to miR-138 antagomiR increased, endogenous aldh1a2 mRNA levels, demonstrating regulation of aldh1a2 by miR-138 in vivo (Fig. 4B)}
{Transfection of decidual cells with anti-miR-338 induced a 2.8-fold reduction in miR- 338 expression (Figures 3A and 3B), while increasing PLA2G4B mRNA 3.7-fold (Figure 3C).immunoblotting also demonstrated an increase in PLA2G4B protein expression in anti-miR-338 transfected cells (Figure 3D)}
{The Northern blot analysis of PMP22 expression reveals a reduction in PMP22 mRNA levels after transfection of miR-9 (Fig. 5A)}
{Using Q-PCR, we found that endogenous c-Myb mRNAwas significantly downregulated to 55% of baseline upon transfection of miR-150 compared to the miR negative control (p=0.008) (Fig. 4A),}
{The decrease in MET mRNA level in these cells (Fig.5D) indicates that miR-1 also induces destabilization of its message.}
{The decrease in MET mRNA level in these cells (Fig.5D) indicates that miR-1 also induces destabilization of its message.}
{Real time RT-PCR analysis demonstrated that ectopic miR-1 reduced the mRNA levels of FoxP1 (Fig. 5E).}
{Significant reduction in endogenous Pim-1 protein (Fig. 5, B andC) andRNAlevels (Fig.5G) in miR-1-expressing cells indicates its negative regulation by miR-1 in A549 cells.}
{In accord with classical miRNA activity, c-myb mRNA levels in cells transfected with miR-15a were not significantly decreased compared with control cell steady state mRNA levels (Figure 3B).}
{In accord with classical miRNA activity, c-myb mRNA levels in cells transfected with miR-15a were not significantly decreased compared with control cell steady state mRNA levels (Figure 3B).}
{We did not find any effects of psilencer-mir-126 on IRS-1 mRNA level (Fig. 3D),}
{RT-PCR showed that miR-183 expression could not decrease mRNA level of VIL2 (data not shown),}
{RT-PCR verified that the mRNA level of KRTAP3-2and RUNX1T1, the most obviously miR-183-responding genes,could be down-regulated by over-expression of miR-183 (data not shown), implying that miR-183 did regulate KRTAP3-2and RUNX1T1 expression.}
{RT-PCR verified that the mRNA level of KRTAP3-2and RUNX1T1, the most obviously miR-183-responding genes,could be down-regulated by over-expression of miR-183 (data not shown), implying that miR-183 did regulate KRTAP3-2and RUNX1T1 expression.}
{Cells transfected with anti-miR-320 expressed lower amounts of miR-320, whereas POLR3D expression was increased in the quiescent state, suggesting that miR-320 might directly regulate transcriptional silencing of POLR3D expression upon cell cycle arrest (Fig. 3)}
{As shown in Figure 5,the expression level of ZFHX1B was significantly down-regulated after transfection.}
{As shown in Figure 5,the expression level of ZFHX1B was significantly down-regulated after transfection.}
{to assess the relative expression levels of CDKN1A and TP53INP1, we carried out RQ-PCR analyses in cells transfected with miR-17-19b-1 or empty vector.We found that expression of both CDKN1A and TP53INP1 is down-regulated in SUDHL4 cells transfected with miR17-19b-1 (referred to as SUDHL4-m1 and SUDHL4-m2), compared with cells transfected with empty vector (referred to as SUDHL4-c1 and SUDHL4-c2)(Figure 3B).}
{Northern blot data confirmed the slight derepression of Cxcl12 as result of LNA-antimiR-140 treatment and the strong repression by siR-140 (Fig. 4A).}
{Meis1 protein and constant MEIS1 mRNA levels were observed in MIRN155-transfected MK cells (Fig 5C).}
{We found that increasingmir-218 levels in H1299 cells caused significant decreases in all 5 genes, but in NHBE cells only 3 (ECOP, NAC-1, and LASP1) of the 5 genes were significantly repressed (Fig. S5A and Fig. S6A). The remaining two targets (MAFG, NFE2L1) are expressed at very low levels at baseline in NHBE cells compared with H1299 cells.}
{We found that increasingmir-218 levels in H1299 cells caused significant decreases in all 5 genes, but in NHBE cells only 3 (ECOP, NAC-1, and LASP1) of the 5 genes were significantly repressed (Fig. S5A and Fig. S6A). The remaining two targets (MAFG, NFE2L1) are expressed at very low levels at baseline in NHBE cells compared with H1299 cells.}
{We found that increasingmir-218 levels in H1299 cells caused significant decreases in all 5 genes, but in NHBE cells only 3 (ECOP, NAC-1, and LASP1) of the 5 genes were significantly repressed (Fig. S5A and Fig. S6A). The remaining two targets (MAFG, NFE2L1) are expressed at very low levels at baseline in NHBE cells compared with H1299 cells.}
{We found that increasingmir-218 levels in H1299 cells caused significant decreases in all 5 genes, but in NHBE cells only 3 (ECOP, NAC-1, and LASP1) of the 5 genes were significantly repressed (Fig. S5A and Fig. S6A). The remaining two targets (MAFG, NFE2L1) are expressed at very low levels at baseline in NHBE cells compared with H1299 cells.}
{We found that increasingmir-218 levels in H1299 cells caused significant decreases in all 5 genes, but in NHBE cells only 3 (ECOP, NAC-1, and LASP1) of the 5 genes were significantly repressed (Fig. S5A and Fig. S6A). The remaining two targets (MAFG, NFE2L1) are expressed at very low levels at baseline in NHBE cells compared with H1299 cells.}
{no significant changes in the ATXN1 or STC1 mRNA levels were observed in the cells transfected with the miR-101b or its inhibitor (Figure 4d).}
{no significant changes in the ATXN1 or STC1 mRNA levels were observed in the cells transfected with the miR-101b or its inhibitor (Figure 4d).}
{Real-time PCR and Western blots revealed significantly increased expression of both RXRa mRNA and protein in activated HSCs cotransfected by anti-miR-27a and anti-miR-27b (Fig. 5)}
{Real-time PCR and Western blots revealed significantly increased expression of both RXRa mRNA and protein in activated HSCs cotransfected by anti-miR-27a and anti-miR-27b (Fig. 5)}
{miR-1 overexpression in NRVM decreased Mef2a protein (Fig. 7d). Mef2a mRNA was downregulated by miR-1 overexpression, suggesting that miR-1 decreased Mef2a transcript stability (Fig. 7e).}
{miR-1 overexpression in NRVM decreased Mef2a protein (Fig. 7d). Mef2a mRNA was downregulated by miR-1 overexpression, suggesting that miR-1 decreased Mef2a transcript stability (Fig. 7e).}
{overexpression did not affect Calm1 mRNA abundance and weakly reduced Calm2 mRNA,}
{overexpression did not affect Calm1 mRNA abundance and weakly reduced Calm2 mRNA,}
{At the same time, real-time RT-PCR analysis of the same transfected cells indicated that c-Myc mRNA was also suppressed by ~50% in the miR-145 transfected cells as compared with vector control (Fig. S5A).}
{Transfection of the pre-miR-29b, but not the scrambled controls, resulted in a marked reduction of the endogenous mRNA levels of DNMT3A and 3B for all 3 cell lines (Figures 1A and B).}
{ectopic expression of pre-miR-29b in AML cell lines and in primary AML blasts induced down-regulation of endogenous Sp1 mRNA and protein compared with scrambled oligonucleotides (Figure 3C and D).}
{Transfection of the pre-miR-29b, but not the scrambled controls, resulted in a marked reduction of the endogenous mRNA levels of DNMT3A and 3B for all 3 cell lines (Figures 1A and B).}
{real-time RT-PCR analysis for the same cells transfected with miR-30e and miR-30c, and found that these two microRNAs had no effect on the Ubc9 mRNA level (Fig.2C),}
{real-time RT-PCR analysis for the same cells transfected with miR-30e and miR-30c, and found that these two microRNAs had no effect on the Ubc9 mRNA level (Fig.2C),}
{real-time RT-PCR analysis for the same cells transfected with miR-30e and miR-30c, and found that these two microRNAs had no effect on the Ubc9 mRNA level (Fig.2C),}
{real-time RT-PCR analysis for the same cells transfected with miR-30e and miR-30c, and found that these two microRNAs had no effect on the Ubc9 mRNA level (Fig.2C),}
{The observation that ZEB2 mRNA levels were significantly reduced (~55.9% F 7.8% and 44.2% F 19.1% in DU145 and PC-3 cells, respectively) upon transfection with pre-205 (Fig. 4B)}
{Microarray data showed down-regulation of PKCq mRNA in pre205-transfected compared with preNeg-transfected DU145 cells (Supplementary Table S5).}
{No change in LMNB1 mRNA levels was noted (data not shown). }
{No change in LMNB1 mRNA levels was noted (data not shown). }
{No change in LMNB1 mRNA levels was noted (data not shown). }
{No change in LMNB1 mRNA levels was noted (data not shown). }
{No change in LMNB1 mRNA levels was noted (data not shown). }
{No change in LMNB1 mRNA levels was noted (data not shown). }
{Over-expression of miR-181a caused a 5-fold reduction of p27  protein levels, while the amount of p27 mRNA was reduced only ~1.5-fold (Fig.7C and D).}
{The down-regulation of endogenous microRNA-21 with anti‚ÄìmicroRNA-21 (Fig. 5A) led to a significant increase in PDCD4 protein (Fig. 5C and D) without any change in PDCD4 mRNA (Fig. 5B).}
{As shown in Figure 3B (left) enforced miR-223 expression resulted in degradation of LMO2 mRNA, as well as treatment with siLMO2}
{A corresponding reduction in APC mRNA levels was detected by qRT-PCR, suggesting mRNA decay as a mechanism involved in miR-135a&b‚Äìmediated APC regulation (Fig. 2B)}
{A corresponding reduction in APC mRNA levels was detected by qRT-PCR, suggesting mRNA decay as a mechanism involved in miR-135a&b‚Äìmediated APC regulation (Fig. 2B)}
{In addition to the protein changes, we also detected a significant decrease of Ezh2 mRNA in PC-3 cells transfected by miR-101 compared to the cells transfected by miR-cont (30% ¬± 15, p <0.05, Fig. 3F).}
{In addition to the protein changes, we also detected a significant decrease of Ezh2 mRNA in PC-3 cells transfected by miR-101 compared to the cells transfected by miR-cont (30% ¬± 15, p <0.05, Fig. 3F).}
{Totally 2 cell cycle related genes, cyclin D1 and p27, were found altered. A strong reduction in the expression of cyclin D1 and increased level of p27 was observed in miR-296 antagomir cells.The results were further confirmed by Western blot.}
{Totally 2 cell cycle related genes, cyclin D1 and p27, were found altered. A strong reduction in the expression of cyclin D1 and increased level of p27 was observed in miR-296 antagomir cells.}
{To evaluate whether MDR1 was a genuine target of miR-296, we analyzed the expression correlation of miR-296 and MDR1 in miR-296 antagomir and control cells by real-time PCR (Fig. 4A) and Western blot (Fig. 4B). The results showed that down-regulation of miR-296 significantly decreased expression of MDR1.}
{As shown in Figure 4A and B,the expression of Bcl-2 was decreased and the expression of Bax was increased in response to down-regulation of miR-296. However, relatively equal levels of Bcl-xL and Bak were detected in all ECA109 derived cell lines.}
{As shown in Figure 4A and B,the expression of Bcl-2 was decreased and the expression of Bax was increased in response to down-regulation of miR-296. However, relatively equal levels of Bcl-xL and Bak were detected in all ECA110 derived cell lines.}
{The inhibition of miR-199a-3p in SNU475 cells determined an increase of both mTOR and P-S6 proteins, with no variations in the mRNA level (Fig. 2C).}
{Expression of endogenous TBP in mRNA as well as protein level was decreased in STHdhQ111/HdhQ111 cells expressing exogenous miR-146a (Fig. 4B and C).}
{Only a slight reduction of DHFR or TS mRNAs expression was observed in HCT 116 (wtp53) cells (Additional file 4A-B), and the results in U-2 OS cells were consistent with HCT 116 (wt-p53) cells.}
{Only a slight reduction of DHFR or TS mRNAs expression was observed in HCT 116 (wtp53) cells (Additional file 4A-B), and the results in U-2 OS cells were consistent with HCT 116 (wt-p53) cells.}
{Only a slight reduction of DHFR or TS mRNAs expression was observed in HCT 116 (wtp53) cells (Additional file 4A-B), and the results in U-2 OS cells were consistent with HCT 116 (wt-p53) cells.}
{p53 mRNA levels were reduced in miR-1285 transfected cells compared to negative controls.}
{p53 mRNA levels were reduced in miR-1285 transfected cells compared to negative controls.}
{A significant decrease of AKT2 mRNA was observed over three time points (24, 48 and 72 hrs) following transfection of miR-184 mimics into Kelly (P =0.004)(Figure 4a) and SK-N-AS (P = 0.003)(Figure 4b).}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{We conducted in vitro miR-204 gain-of-function analyses by transiently transfecting JSQ3 and SQ38 HNSCC cells with mature miR-204 mimics (Dharmacon) to enhance miR-204 function in these two cell lines. Restoration of miR-204 function achieved significant inhibition (between 30% to 75%) of endogenous mRNA expression in 18 outof 21 predicted targets examined for both cell lines, while nonspecific control mimics had no significant effect.}
{"The miR-31 targets sought were those that were repressed by forced miR-31 overexpression and augmented by its engineered knockdown in lung cancer cells."}
{"The miR-31 targets sought were those that were repressed by forced miR-31 overexpression and augmented by its engineered knockdown in lung cancer cells."}
{"The miR-31 targets sought were those that were repressed by forced miR-31 overexpression and augmented by its engineered knockdown in lung cancer cells."}
{"The miR-31 targets sought were those that were repressed by forced miR-31 overexpression and augmented by its engineered knockdown in lung cancer cells."}
{Transfection of pre-miR27b or pre-miR128a decreased A2BAR mRNA levels by 50% compared with untransfected cells (pre-miR27b 43.4 4.83, *p   0.001; pre-miR128a 30.3   6.1, *p   0.003), whereas 18S mRNA (control) was unaffected by pre-miR27b or premiR128a transfection.}
{Transfection of pre-miR27b or pre-miR128a decreased A2BAR mRNA levels by 50% compared with untransfected cells (pre-miR27b 43.4 4.83, *p   0.001; pre-miR128a 30.3   6.1, *p   0.003), whereas 18S mRNA (control) was unaffected by pre-miR27b or premiR128a transfection.}
{anti-miR27b and anti-miR128a increasedA2BARmRNAlevels by 5.3 0.9-fold (*p 0.01) and 2.2   0.02-fold (*p   0.005), respectively, compared with vector-transfected cells. 18S mRNA did not change.}
{We found that, interestingly, both IL-10 mRNA and protein levels were higher in the miR-466loverexpressed RAW264.7 cells than that in mock control cells when these cells were stimulated with TLR ligands (Fig. 2B‚ÄìD; Supplemental Fig. 1).}
{Indeed, Btg2 messenger RNA (mRNA) levels and activity of a reporter gene linked to its 30UTR readily responded to miR-21 mimic or inhibitor transfection into well-differentiated mouse hepatoma cells (Fig. 3C).}
{Indeed, Btg2 messenger RNA (mRNA) levels and activity of a reporter gene linked to its 30UTR readily responded to miR-21 mimic or inhibitor transfection into well-differentiated mouse hepatoma cells (Fig. 4C).}
{We examined the differences in miR-155 and CYR61 expression levels between the control and PE placentas by quantitative real time reverse transcriptase-polymerase chain reaction (qRT-PCR) (Figure 1, A). The expression of miR-155 in severe PE placenta is 2.58-fold higher in comparison to the control placentas (P  <0.001). The transcript level of CYR61 was significantly lower in severe PE placenta compared to the control group (Figure 1, A) (P <0.01).}
{It is noteworthy that both isoforms of YAP contain the same 3'UTR regions, and the results showed that miR-375 was significantly down-regulated in HCC tumor tissues, while both isoforms of YAP were up-regulated in HCC tumor tissues, suggesting YAP is a target of miR-375 (Fig. 1B).}
{AGS cells transfected with miR-155 mimics or miR-155 control. As shown in Fig. 2A, miR-155 has no effect on the Mrna expression level of MyD88.}
{Enforced expression of all three miR-34 family members reduced Myc protein abundance; however, miR-34c was the most potent (Fig. S1E).}
{Enforced expression of all three miR-34 family members reduced Myc protein abundance; however, miR-34c was the most potent (Fig. S1E).}
{Enforced expression of all three miR-34 family members reduced Myc protein abundance; however, miR-34c was the most potent (Fig. S1E).}
{These genes were up-regulated in the AMKL cell lines upon miR-125b knockdown and down-regulated in HSPC upon miR-125b-2 overexpression (Fig. 5A; Supplemental Fig. S6).}
{These genes were up-regulated in the AMKL cell lines upon miR-125b knockdown and down-regulated in HSPC upon miR-125b-2 overexpression (Fig. 5A; Supplemental Fig. S6).}
{Interestingly, the reduction in ERa protein levels was markedly greater than the reduction in ESR1 mRNA levels determined by quantitative RT-PCR (Fig. 2G).}
{No change of PTEN mRNA was observed.}
{Overexpression of miR-143 resulted in a ~3-fold decrease in add3 transcript levels (P=0.0001).}
{However, RT-PCR analysis revealed that FOXO3a mRNA levels remained unchanged (Fig. 2B and 2C).}
{Moreover, qRT-PCR analyses showed that the SOCS1 mRNA level was downregulated by ‚àº30% when miR-155 was overexpressed ‚àº16-fold.}
{De-repression of the CTGF transcript was observed after anti-miR-18a transfection (Figure 4e).}
{In our dataset, expression of miR-18a, miR- 19a and miR-19b was inversely correlated with Mrna expression of CTGF (Table 3). Separate analysis of the five GBIV cultures showed differences in induction response patterns (Figures 4a‚Äìd).}
{In our dataset, expression of miR-18a, miR- 19a and miR-19b was inversely correlated with Mrna expression of CTGF (Table 3). Separate analysis of the five GBIV cultures showed differences in induction response patterns (Figures 4a‚Äìd).}
{Since Jak1 was efficiently down-regulated on mRNA as well as on protein level by miR-17 and the closely related miR-20a (Fig. 5A/B/C)}
{Overexpression of miR-17 significantly reduced several predicted targets, including the cell cycle inhibitor p21, the S1P receptor EDG1, and the protein kinase Jak1.}
{Overexpression of miR-17 significantly reduced several predicted targets, including the cell cycle inhibitor p21, the S1P receptor EDG1, and the protein kinase Jak1.}
{Since Jak1 was efficiently down-regulated on mRNA as well as on protein level by miR-17 and the closely related miR-20a (Fig. 5A/B/C)}
{First we showed by Northern blot analysis that the mRNA level of Smad3 remained unchanged after manipulation of miR-140 activity (Fig. 1A).}
{"EGR2 levels were also up-regulated in gastricimmortal epithelial cells compared to cancerous cell lines (Fig. 3B)."}
{As shown in Figure 2d with quantitative RT-PCR analysis, a significant decrease of RhoC mRNA level was detected in UM1 cells that were transfected with the miR-138 mimic.}
{As shown in Figure 3d, no significant change in ROCK2 mRNA level was detected when cells were transfected with either miR-138 mimic or anti-miR-138 PNA.}
{The downregulation of 14-3-3Œ∂ and cIAP-2 and upregulation of Bim by pre375 were further validated by qRT-PCR (Fig. 3B). As shown in Fig. 3C, 14-3-3Œ∂ was also downregulated at the protein level.}
{"Increased the levels of COL1A1 and COL3A1 mRNA in nonrescued scrambled controls, but this effect was abolished by overexpressionof miR-29a (Figure 5B)."}
{Transfection of anti‚ÄìmiR-135a induced FLAP mRNA expression by 8-fold under hypoxic condition, when compared with hypoxia alone (Fig. 7D, lane 3 versus lane 2) in t-HBEC.}
{Transfection with anti‚ÄìmiR-199a-5p induced FLAP mRNA expression by 4-fold over and above treatment with hypoxia alone (Fig. 7D, lane 4 versus lane 2).}
{The three miR-128 targeted proteins LDLR, TXNIP, and DBI (Fig. 5) were effectively knocked-down by miR-128 transfections.}
{The three miR-128 targeted proteins LDLR, TXNIP, and DBI (Fig. 5) were effectively knocked-down by miR-128 transfections.}
{The three miR-128 targeted proteins LDLR, TXNIP, and DBI (Fig. 5) were effectively knocked-down by miR-128 transfections.}
{LDLR was also strongly reduced by miR-124 transfection.}
{AGO2 mRNA levels were significantly decreased in cell lysates following miR-107 and miR-128 transfection. AGO1 and AGO3 mRNA was also decreased (Fig. 7A) in miR-107 transfection.}
{AGO2 mRNA levels were significantly decreased in cell lysates following miR-107 and miR-128 transfection. AGO1 and AGO3 mRNA was also decreased (Fig. 7A) in miR-107 transfection.}
{AGO2 mRNA levels were significantly decreased in cell lysates following miR-107 and miR-128 transfection. AGO1 and AGO3 mRNA was also decreased (Fig. 7A) in miR-107 transfection.}
{AGO2 mRNA levels were significantly decreased in cell lysates following miR-107 and miR-128 transfection. AGO1 and AGO3 mRNA was also decreased (Fig. 7A) in miR-107 transfection.}
{There was no reduction in DHFR mRNA expression associated with miR-24 overexpression.}
{The results showed that the cells treated with the miR-133a mimic decreased NFATc4 mRNA levels 65% compared with cells treated with the control mimic (P <  0.05) (Fig. 3A). }
{The results showed that the cells treated with the miR-133a mimic decreased NFATc4 mRNA levels 65% compared with cells treated with the control mimic (P <  0.05) (Fig. 3A). }
{We utilized quantitative RT-PCR to measure the levels of Peli1 mRNA during liver regeneration. At 12 h, as miR-21 levels peak, we observed a statistically significant reduction in Peli1 mRNA levels (Fig. 2B).}
{In line, transfection with the miR-27b mimic reduced PPAR 1 mRNA in a concentration-dependent manner (Fig. 6A).}
{Western blot and qPCR experiments confirmed that miR-221 represses DDIT4 expression at both the protein and RNA levels in the different cell types (Fig. 5C and Fig. S6D).}
{Western blot and qPCR experiments confirmed that miR-221 represses DDIT4 expression at both the protein and RNA levels in the different cell types (Fig. 5C and Fig. S6D).}
{A similar decrease was observed for BNIP3L and TBK1 protein/RNA levels, although the effect of miR-221 was weaker for these two targets (Fig. 5C and Fig. S6D).}
{A similar decrease was observed for BNIP3L and TBK1 protein/RNA levels, although the effect of miR-221 was weaker for these two targets (Fig. 5C and Fig. S6D).}
{Transfectionwith 30 nMof premiR-494 resulted in a decrease in PTEN protein (Fig. 2A and B) while mRNA remained unchanged (Fig. 2C) in both 16HBE-T30 and 16HBEN30 cells.}
{Transfectionwith 30 nMof premiR-494 resulted in a decrease in PTEN protein (Fig. 2A and B) while mRNA remained unchanged (Fig. 2C) in both 16HBE-T30 and 16HBEN30 cells.}
{QPCR analyses showed that transfections with any of these miRs did not affect KRT mRNA levels in the cells.}
{QPCR analyses showed that transfections with any of these miRs did not affect KRT mRNA levels in the cells.}
{QPCR analyses showed that transfections with any of these miRs did not affect KRT mRNA levels in the cells.}
{QPCR analyses showed that transfections with any of these miRs did not affect KRT mRNA levels in the cells.}
{Ectopic expression of the miR-331 reduced the CDCA5 level by 44% in VCaP and 48% in LNCaP cells, and the KIF23 level by 43% in VCaP and 44% in LNCaP cells (Fig. 3A).}
{Ectopic expression of the miR-331 reduced the CDCA5 level by 44% in VCaP and 48% in LNCaP cells, and the KIF23 level by 43% in VCaP and 44% in LNCaP cells (Fig. 3A).}
{Treatment with pre-miR-140 significantly inhibited (p = 0.0002) IGFBP-5 expression at as early as 24 hours (Figure 4A).}
{3 genes (CCNA2, PA2G4, and BRCA1) were downregulated after PMA treatment; however, their expression was rescued upon miR-146a inhibition (Fig. 2B).}
{3 genes (CCNA2, PA2G4, and BRCA1) were downregulated after PMA treatment; however, their expression was rescued upon miR-146a inhibition (Fig. 2B).}
{3 genes (CCNA2, PA2G4, and BRCA1) were downregulated after PMA treatment; however, their expression was rescued upon miR-146a inhibition (Fig. 2B).}
{"As shown in Fig.2b, CCNE1 mRNA levels in cells transfected with miR-16-1 overexpression plasmid were correspondingly decreased about60% compared to that in cells transfected with the control plasmid."}
{"As shown in Fig.2b, CCNE1 mRNA levels in cells transfected with miR-16-1 overexpression plasmid were correspondingly decreased about60% compared to that in cells transfected with the control plasmid."}
{By contrast, no change in HDAC5 mRNA levels was noted (Figure 4C).}
{The amount of HNF-6 mRNA was reduced by 50% in the BMEL cells transfected with a miR-495 expression vector, when compared to cells transfected with a vector coding for a scrambled version of miR-495 (Fig. 3C),}
{When overexpressed in BMEL cells, miR-218 was able to reduce by 60% the amount of endogenous OC-2 mRNA, when compared to control (Fig. 3D).}
{When overexpressed in BMEL cells, miR-218 was able to reduce by 60% the amount of endogenous OC-2 mRNA, when compared to control (Fig. 3D).}
{When overexpressed in BMEL cells, miR-218 was able to reduce by 60% the amount of endogenous OC-2 mRNA, when compared to control (Fig. 3D).}
{"In contrast, transfection of miR-218 precursors triggered a negligible change in Col1A1 and SP1 mRNA expression (Fig. 4A, left andright panels) but slightly reduced their protein level (Fig. 4B)."}
{Transient transfection of miR-29b precursors signifi-cantly inhibited type I collagen mRNA and protein expression (Fig. 4A, left panel, and B) in unstimulated human stellate cells.}
{"In contrast, transfection of miR-218 precursors triggered a negligible change in Col1A1 and SP1 mRNA expression (Fig. 4A, left andright panels) but slightly reduced their protein level (Fig. 4B)."}
{Moreover, the transfection of miR-29b precursors decreased SP1 mRNA and protein expression (Fig. 4A, right panel, and B).}
{These cells expressed PTEN, PDCD4, E2F1 and TGF-bRII mRNAs and proteins at varying levels (Figs 3 and 4) and gain- and loss-of-miR-21 function differentially altered their expression in a cell-specific manner when compared with scrambled-oligo-transfected controls.}
{These cells expressed PTEN, PDCD4, E2F1 and TGF-bRII mRNAs and proteins at varying levels (Figs 3 and 4) and gain- and loss-of-miR-21 function differentially altered their expression in a cell-specific manner when compared with scrambled-oligo-transfected controls.}
{These cells expressed PTEN, PDCD4, E2F1 and TGF-bRII mRNAs and proteins at varying levels (Figs 3 and 4) and gain- and loss-of-miR-21 function differentially altered their expression in a cell-specific manner when compared with scrambled-oligo-transfected controls.}
{These cells expressed PTEN, PDCD4, E2F1 and TGF-bRII mRNAs and proteins at varying levels (Figs 3 and 4) and gain- and loss-of-miR-21 function differentially altered their expression in a cell-specific manner when compared with scrambled-oligo-transfected controls.}
{Real-time QPCR confirmed seven downregulated genes (SET, E-Cadherin, EGFR, FOLR1, KRAS, SKP2, and CDC42) in miR-199b overexpressed choriocarcinoma cell lines (Fig. 1).}
{Transfection of pre-miR-218 also caused a reduction in ECOP expression in AGS cells.}
{To establish a link between miR-155 and SHIP1 expression beyond mere correlation, the non- GC-DLBCL cell line OCILY-3 was transfected either with a non-specific control-miR, miR-1 or miR-155. Neither miR-1 nor the control miR affected SHIP1 mRNA levels, whereas introduction of miR-155 resulted in a clear decrease in SHIP1 mRNA (Fig 2A).}
{"In comparison with NC-transfectants, hsa-miR-155-transfected cells revealed a significant reduction (~80%) in the C/EBPÔÅ¢ protein level (Figure 4C, upper panel). Conversely, no fluctuation in C/EBPŒ≤ mRNA levels was observed after miR-155 transfection (Figure 4C,lower panel)."}
{The expression levels of these seven miRNAs and their 13 target mRNAs were found to exhibit highly negative correlations (Table II).}
{The expression levels of these seven miRNAs and their 13 target mRNAs were found to exhibit highly negative correlations (Table II).}
{The expression levels of these seven miRNAs and their 13 target mRNAs were found to exhibit highly negative correlations (Table II).}
{The expression levels of these seven miRNAs and their 13 target mRNAs were found to exhibit highly negative correlations (Table II).}
{The expression levels of these seven miRNAs and their 13 target mRNAs were found to exhibit highly negative correlations (Table II).}
{The expression levels of these seven miRNAs and their 13 target mRNAs were found to exhibit highly negative correlations (Table II).}
{The expression levels of these seven miRNAs and their 13 target mRNAs were found to exhibit highly negative correlations (Table II).}
{Ectopic expression of miR-139 results in a decrease in FoxO1 protein of approximately 30% (Fig. 1D) without affecting FoxO1 mRNA level (Fig. 1C).}
{"Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level ofRECK mRNA."}
{"Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA."}
{"Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA."}
{"Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA."}
{Downregulation of FIH mRNA expression and protein expression was found in SAS-miR-31 cells compared with controls.}
{Downregulation of FIH mRNA expression and protein expression was found in SAS-miR-31 cells compared with controls.}
{"No significant difference in cyclin D1 mRNA levels was observed between the EA.hy.926 cells with stable miR-19a expression and the control cells (Fig. 3B)."}
{No significant change in ICAM-1 mRNA levels was found between the control cells and cells treated with anti-miR-221.}
{PTEN mRNA levels were also determined by qPCR. As in the western blot analysis, when miR-205 was overexpressed, PTEN mRNA levels decreased by approximately 50% as compared with the luciferase shRNA control (Fig. 4F).}
{PTEN mRNA levels were also determined by qPCR. As in the western blot analysis, when miR-205 was overexpressed, PTEN mRNA levels decreased by approximately 50% as compared with the luciferase shRNA control (Fig. 4F).}
{By array analysis, Atp1a1 expression was downregulated 1.8-fold in cells overexpressing miR-205.}
{We also detected a 1.5-fold decrease of docking protein 4 (Dok4) expression by qPCR (Fig. 5B), although array analysis indicated that Dok4 was downregulated to a slightly greater extent (2.2-fold) by miR-205.}
{Consistent with the downregulation of miR-64/65 in transgenic overexpressing lines, we observed significant overexpression of mdl-1 (4-fold), ptc-1 (3-fold).}
{Consistent with the downregulation of miR-64/65 in transgenic overexpressing lines, we observed significant overexpression of mdl-1 (4-fold), ptc-1 (3-fold).}
{Consistent with the downregulation of miR-64/65 in transgenic overexpressing lines, we observed significant overexpression of mdl-1 (4-fold), ptc-1 (3-fold).}
{Consistent with the downregulation of miR-64/65 in transgenic overexpressing lines, we observed significant overexpression of mdl-1 (4-fold), ptc-1 (3-fold).}
{Using qRT-PCR and immunoblotting of p16Ink4a and p19Arf we show that both are downregulated in Lmnb1Œî/Œî compared to WT cells and that transfecting Lmnb1Œî/Œî cells with anti-mir-31 results in the upregulation of both (Fig. 4A and B).}
{The downregulation of NOTCH4 and KRAS and upregulation of p21 (WAF1/Cip1) were observed in drug-treated cells (Figure 5D).}
{The downregulation of NOTCH4 and KRAS and upregulation of p21 (WAF1/Cip1) were observed in drug-treated cells (Figure 5D).}
{Real time quantitative PCR of KLF4 mRNA showed that miR-10b overexpression or inhibition had no effect on KLF4 mRNA level (Fig. 4B).}
{"Cells with enforced expression of miR-200a or the miR-200b cluster exhibited reduced levels of ZEB1 and ZEB2 mRNAs (Fig.4E). "}
{"Cells with enforced expression of miR-200a or the miR-200b cluster exhibited reduced levels of ZEB1 and ZEB2 mRNAs (Fig.4E). "}
{The level of Hes-1 mRNA was unchanged.}
{TIMP3 RNA level was also dramatically reduced (B70%) in both cell lines by miR-181b.}
{miR-15b down-regulated both mRNA and protein of Arl2. }
{Arl2 mRNA levels were maximally decreased to almost similar levels amongmiR-15b, -16, -195, and -424.}
{Arl2 mRNA levels were maximally decreased to almost similar levels amongmiR-15b, -16, -195, and -424.}
{Arl2 mRNA levels were maximally decreased to almost similar levels amongmiR-15b, -16, -195, and -424.}
{ MKK4 mRNA abundance was unchanged after transfecting all four (AS)miRNAs.}
{ MKK4 mRNA abundance was unchanged after transfecting all four (AS)miRNAs.}
{ MKK4 mRNA abundance was unchanged after transfecting all four (AS)miRNAs.}
{ MKK4 mRNA abundance was unchanged after transfecting all four (AS)miRNAs.}
{ Let-7c was capable of inhibiting the expression of both HMGA2 (a known target of let-7c [37]) and TGFBR1 mRNAs.}
{ Let-7c was capable of inhibiting the expression of both HMGA2 (a known target of let-7c [37]) and TGFBR1 mRNAs.}
{We found that the mRNA level of SIP1 was not changed while the protein level of SIP1 was down-regulated after overexpression .}
{We found that the mRNA level of SIP1 was not changed while the protein level of SIP1 was down-regulated after overexpression .}
{Whereas induction of PPARc and C/ EBPa during early onset of adipogenesis was blunted by miR-27b. }
{"Among 532 target genes, the mRNA levels of 10 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood. "}
{Among 532 target genes, the mRNA levels of 11 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 12 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 13 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 14 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 15 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 16 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 17 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 18 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 19 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 20 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 21 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 22 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 23 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 24 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 25 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 26 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 27 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 28 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 29 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{Among 532 target genes, the mRNA levels of 30 predicted gene targets were down-regulated in adult blood compared to umbilical cord blood.}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-146a in miRBase Targets. "}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-147a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-149a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-150a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-151a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-152a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-154a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-155a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-156a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-157a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-158a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-159a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-160a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-161a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-162a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-163a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-164a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-165a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-166a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-167a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-168a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-169a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-170a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-172a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-173a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-174a in miRBase Targets."}
{"We found 337 transcripts that were significantly downregulated after PMA treatment but were rescued upon miR-146a inhibition. Among them, 29 genes were the predicted targets of miR-169a in miRBase Targets."}
{Interestingly, the overexpression of miR-155 with RCAS(A)miR-155 downregulated JARID2 mRNA to 40% of the level in uninfected and control infected cells (Fig. 3).}
{Interestingly, the overexpression of miR-155 with RCAS(A)miR-155 downregulated JARID2 mRNA to 40% of the level in uninfected and control infected cells (Fig. 3).}
{The expression of 133a and 133b reduced the protein levels of KLF15, whereas they did not change the KLF15 mRNA level.}
{The expression of 133a and 133b reduced the protein levels of KLF15, whereas they did not change the KLF15 mRNA level.}
{Interestingly, we found that increased levels of miR-200a in meningioma cells significantly downregulated  -catenin at both mRNA and protein levels.}
{A significant reduction by LV-miR-124 of BDNF mRNA levels of 22, 47, and 49% was found by qRT-PCR.}
{A significant downregulation was observed from qRT-PCR with reduction in DA D3R mRNA levels of 29, 41, and 41%.}
{As a result, when miR-9 was blocked, NF-jB1 mRNA was elevated compared with the control group, with an 80% increase.}
{Real time RT-PCR using total cell RNA harvested at the indicated time points revealed that whereas let-7e inhibits, as-let-7e enhances the expression of TLR4.}
{Real time RT-PCR using total cell RNA harvested at the indicated time points, revealed that as-miR-155 enhanced the expression of SOCS1 both in na√Øve (Figure 4D) and LPS-activated (Figure 4E) RAW264.7 cells.}
{For miR-107, we confirmed mRNA down-regulation of CCNE1 (NM_001238), CDK6, CDCA4 (NM_017955.3), RAB1B (NM_030981.2) and CRKL (NM_005207.3).}
{For miR-107, we confirmed mRNA down-regulation of CCNE1 (NM_001238), CDK6, CDCA4 (NM_017955.3), RAB1B (NM_030981.2) and CRKL (NM_005207.3).}
{For miR-107, we confirmed mRNA down-regulation of CCNE1 (NM_001238), CDK6, CDCA4 (NM_017955.3), RAB1B (NM_030981.2) and CRKL (NM_005207.3).}
{For miR-107, we confirmed mRNA down-regulation of CCNE1 (NM_001238), CDK6, CDCA4 (NM_017955.3), RAB1B (NM_030981.2) and CRKL (NM_005207.3).}
{For miR-107, we confirmed mRNA down-regulation of CCNE1 (NM_001238), CDK6, CDCA4 (NM_017955.3), RAB1B (NM_030981.2) and CRKL (NM_005207.3).}
{For miR-107, we confirmed mRNA down-regulation of CCNE1 (NM_001238), CDK6, CDCA4 (NM_017955.3), RAB1B (NM_030981.2) and CRKL (NM_005207.3).}
{For miR-185, we confirmed down-regulation of CCNE1, CDK6, AKT1 (NM_001014431.1),HMGA2 (NM_003483.4) and CORO2B (NM_006091.3) (Fig. 5B).}
{For miR-185, we confirmed down-regulation of CCNE1, CDK6, AKT1 (NM_001014431.1),HMGA2 (NM_003483.4) and CORO2B (NM_006091.3) (Fig. 5B).}
{For miR-185, we confirmed down-regulation of CCNE1, CDK6, AKT1 (NM_001014431.1),HMGA2 (NM_003483.4) and CORO2B (NM_006091.3) (Fig. 5B).}
{For miR-185, we confirmed down-regulation of CCNE1, CDK6, AKT1 (NM_001014431.1),HMGA2 (NM_003483.4) and CORO2B (NM_006091.3) (Fig. 5B).}
{For miR-185, we confirmed down-regulation of CCNE1, CDK6, AKT1 (NM_001014431.1),HMGA2 (NM_003483.4) and CORO2B (NM_006091.3) (Fig. 5B).}
{Because the level of Bmf mRNA expression did not change in response to miR-221 or anti-miR-221, our results show that the control of Bmf expression is at the translational level.}
{FUS1 mRNA levels are not significantly affected by miRNA over-expression}
{Expression of all three-target genes by quantitative RT-PCR responded as expected with suppression of between 50 and 80% in response to elevated miR-17 or miR-20a (Fig. 5).}
{Expression of all three-target genes by quantitative RT-PCR responded as expected with suppression of between 50 and 80% in response to elevated miR-17 or miR-20a (Fig. 5).}
{Expression of all three-target genes by quantitative RT-PCR responded as expected with suppression of between 50 and 80% in response to elevated miR-17 or miR-20a (Fig. 5).}
{Expression of all three-target genes by quantitative RT-PCR responded as expected with suppression of between 50 and 80% in response to elevated miR-17 or miR-20a (Fig. 5).}
{Expression of all three-target genes by quantitative RT-PCR responded as expected with suppression of between 50 and 80% in response to elevated miR-17 or miR-20a (Fig. 5).}
{Expression of all three-target genes by quantitative RT-PCR responded as expected with suppression of between 50 and 80% in response to elevated miR-17 or miR-20a (Fig. 5).}
{We could more clearly predict that mRNA transcript levels of the c14orf24, LAMC1, PTBP1, PTPN12 and LMNB1 genes were significantly and directly repressed by miR124a, indicating that mRNA of the five target genes was destabilized by miR124a (Fig. 3C).}
{We could more clearly predict that mRNA transcript levels of the c14orf24, LAMC1, PTBP1, PTPN12 and LMNB1 genes were significantly and directly repressed by miR124a, indicating that mRNA of the five target genes was destabilized by miR124a (Fig. 3C).}
{We could more clearly predict that mRNA transcript levels of the c14orf24, LAMC1, PTBP1, PTPN12 and LMNB1 genes were significantly and directly repressed by miR124a, indicating that mRNA of the five target genes was destabilized by miR124a (Fig. 3C).}
{We could more clearly predict that mRNA transcript levels of the c14orf24, LAMC1, PTBP1, PTPN12 and LMNB1 genes were significantly and directly repressed by miR124a, indicating that mRNA of the five target genes was destabilized by miR124a (Fig. 3C).}
{We could more clearly predict that mRNA transcript levels of the c14orf24, LAMC1, PTBP1, PTPN12 and LMNB1 genes were significantly and directly repressed by miR124a, indicating that mRNA of the five target genes was destabilized by miR124a (Fig. 3C).}
{The results showed that miR-155 mimics decreased the mRNA levels of IKK- Œµ and SMAD2.}
{The results showed that miR-155 mimics decreased the mRNA levels of IKK- Œµ and SMAD2.}
{In contrast, no significant difference was found for FADD mRNA.}
{Stabilization of Œ≤TrCP1 mRNA by anti-miR-183 resulted in increased levels of endogenous Œ≤TrCP1 (but not its homologue, Œ≤TrCP2) mRNA in several cell lines tested (Figure 2e).}
{We showed that expressions between miR-143 and DNMT3A mRNA were inversely correlated in all 10 paired CRC.}
{Consistent with the microarray data, the depletion of three of these, Clathrin Interactor 1(CLINT1), core-binding factor b subunit (CBFB), and protein phosphatase 3 catalytic subunit a isoform (PPP3CA) was also observed by RT‚ÄìQpcr(Figure 6d).}
{Consistent with the microarray data, the depletion of three of these, Clathrin Interactor 1(CLINT1), core-binding factor b subunit (CBFB), and protein phosphatase 3 catalytic subunit a isoform (PPP3CA) was also observed by RT‚ÄìQpcr(Figure 6d).}
{Consistent with the microarray data, the depletion of three of these, Clathrin Interactor 1(CLINT1), core-binding factor b subunit (CBFB), and protein phosphatase 3 catalytic subunit a isoform (PPP3CA) was also observed by RT‚ÄìQpcr(Figure 6d).}
{Bioinformatic analysis identified nine mRNAs that were (1) expressed above a background level in untreated cells, (2) downregulated at 46 h, (3) containing a 7mer target site, and (4) predicted targets (TargetScan/PicTar) (Figure 6c, gray shadow and S3).}
{Bioinformatic analysis identified nine mRNAs that were (1) expressed above a background level in untreated cells, (2) downregulated at 46 h, (3) containing a 7mer target site, and (4) predicted targets (TargetScan/PicTar) (Figure 6c, gray shadow and S3).}
{Bioinformatic analysis identified nine mRNAs that were (1) expressed above a background level in untreated cells, (2) downregulated at 46 h, (3) containing a 7mer target site, and (4) predicted targets (TargetScan/PicTar) (Figure 6c, gray shadow and S3).}
{Bioinformatic analysis identified nine mRNAs that were (1) expressed above a background level in untreated cells, (2) downregulated at 46 h, (3) containing a 7mer target site, and (4) predicted targets (TargetScan/PicTar) (Figure 6c, gray shadow and S3).}
{Bioinformatic analysis identified nine mRNAs that were (1) expressed above a background level in untreated cells, (2) downregulated at 46 h, (3) containing a 7mer target site, and (4) predicted targets (TargetScan/PicTar) (Figure 6c, gray shadow and S3).}
{Bioinformatic analysis identified nine mRNAs that were (1) expressed above a background level in untreated cells, (2) downregulated at 46 h, (3) containing a 7mer target site, and (4) predicted targets (TargetScan/PicTar) (Figure 6c, gray shadow and S3).}
{With transfection of either the miR-155 or -802 mimic, endogenous miR-155 and -802 levels increased by 200‚Äì310% (Fig. 1G) and MeCP2 mRNA (Fig. 1G) and MeCP2 protein (Fig. 1H) levels were significantly decreased (30‚Äì50% at the mRNA level and 40‚Äì50% at the protein level).}
{With transfection of either the miR-155 or -802 mimic, endogenous miR-155 and -802 levels increased by 200‚Äì310% (Fig. 1G) and MeCP2 mRNA (Fig. 1G) and MeCP2 protein (Fig. 1H) levels were significantly decreased (30‚Äì50% at the mRNA level and 40‚Äì50% at the protein level).}
{With transfection of either the miR-155 or -802 mimic, endogenous miR-155 and -802 levels increased by 200‚Äì310% (Fig. 1G) and MeCP2 mRNA (Fig. 1G) and MeCP2 protein (Fig. 1H) levels were significantly decreased (30‚Äì50% at the mRNA level and 40‚Äì50% at the protein level).}
{With transfection of either the miR-155 or -802 mimic, endogenous miR-155 and -802 levels increased by 200‚Äì310% (Fig. 1G) and MeCP2 mRNA (Fig. 1G) and MeCP2 protein (Fig. 1H) levels were significantly decreased (30‚Äì50% at the mRNA level and 40‚Äì50% at the protein level).}
{We found that miR-7 significantly reduced hCD98 mRNA levels in Caco2-BBE cells at 24 and 48 h post-transfection (Fig. 3A).}
{As shown in Fig. 3, D and E, miR-706 significantly down-regulated expression of mCD98 at both mRNA and protein levels after 1 and 2 days of transfection.}
{Using real time RT-PCR, we found that miR-125a transfection did not significantly change HuR mRNA level in MCF-7 cells (Fig. 6A).}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{As shown in Figure 4, ectopic transfection of synthetic miR-29a or -29b resulted in downregulation of MCL-1 (Figure 4A), CXXC6 (Figure 4B), and CDK6 (Figure 4C) mRNA levels with respect to the controls at 24 hours.}
{modest but statistically insignificant changes in the levels of mRNA as assessed by TaqmanTM real time RT-PCR.}
{modest but statistically insignificant changes in the levels of mRNA as assessed by TaqmanTM real time RT-PCR.}
{modest but statistically insignificant changes in the levels of mRNA as assessed by TaqmanTM real time RT-PCR.}
{modest but statistically insignificant changes in the levels of mRNA as assessed by TaqmanTM real time RT-PCR.}
{Overexpression of miR200b resulted in a significant decrease in WAVE3 expression compared with the control cells}
{"We found that the cases with the SET8 CC genotype (n = 24), which has the perfect complementary seed sequence for miR-502, had lower levels ofSET8 expression than did cases with the TT genotype (n = 27; P = 0.018; Fig. 3A)."}
{Real-time RT‚ÄìPCR of RIP140 showed that RIP140 mRNAlevels were not affected in P19 cells transfected with either a mir-346 mimic or a mir-346 inhibitor (Figure 3C),}
{qRT-PCR analysis confirmed that E2F2 mRNA was significantly downregulated by overexpressing miR-24.}
{PCR revealed no change in cyclin D1 mRNA levels upon miR-16 addition.}
{In addition, the level of human notch3 mRNA was also repressed by miR-206 (Fig. 2D).}
{On the contrary, reelin mRNA levels were not affected by miR-128 ectopic expression (Fig. 3E, right panel).}
{Moreover, we also measured DCX mRNA levels by Q-RT-PCR in miR-128-transfected cells, and we verified that they were significantly reduced ( 75%) as compared to those measured in control cells (Fig. 3E, left panel).}
{Consistent with the results obtained in microarray analysis, Cdc25A levels were significantly up-regulated in miR-21 knockout cells (Fig. 2A and B).}
{Transfection of MDA-MB-231 cells with 30 nM miR-193b inhibitor caused elevated uPA protein expression (Figure 4a), without affecting the uPA mRNA amounts (Figure 4b).}
{we found that transfection of miR-133b down regulated not only b-III-tubulin but also Pitx3 and IGF-IR(Fig. 4A). Third,we found thatdownregulationof b-III-tubulin, Pitx3 and IGF-Ir by miR-133b occurred at the protein but not the mRNA level(Fig. 4B and C).}
{Compared with the vehicle control, there was a slight increase in Mcl-1 but not Bcl-2 and Bcl-XL mRNA levels in cells transfected with NC or miR-153 (Figs. 3b, 3d and 3f).}
{Compared with the vehicle control, there was a slight increase in Mcl-1 but not Bcl-2 and Bcl-XL mRNA levels in cells transfected with NC or miR-153 (Figs. 3b, 3d and 3f).}
{As shown in Figure 6, an up-regulation of RhoA mRNA and down-regulations of miR- 133a and miR-133a* (a minor miRNA) were observed in BSM tissues of the OA-challenged mice.}
{As shown in Figure 6, an up-regulation of RhoA mRNA and down-regulations of miR- 133a and miR-133a* (a minor miRNA) were observed in BSM tissues of the OA-challenged mice.}
{we observed a significant reduction in expression levels of the PGC marker Dppa-3 indifferentiating ESCs after overexpression of miR 290 cluster(Fig. 4A).}
{we observed a significant reduction in expression levels of the PGC marker Dppa-3 indifferentiating ESCs after overexpression of miR 290 cluster(Fig. 4A).}
{we observed a significant reduction in expression levels of the PGC marker Dppa-3 indifferentiating ESCs after overexpression of miR 290 cluster(Fig. 4A).}
{we observed a significant reduction in expression levels of the PGC marker Dppa-3 indifferentiating ESCs after overexpression of miR 290 cluster(Fig. 4A).}
{we observed a significant reduction in expression levels of the PGC marker Dppa-3 indifferentiating ESCs after overexpression of miR 290 cluster(Fig. 4A).}
{we observed a significant reduction in expression levels of the PGC marker Dppa-3 indifferentiating ESCs after overexpression of miR 290 cluster(Fig. 4A).}
{Furthermore, transfection of miR-146a mimics decreased IRAK2 expression in macrophages at both the protein and mRNA levels.}
{Furthermore, transfection of miR-146a mimics decreased IRAK2 expression in macrophages at both the protein and mRNA levels.}
{Furthermore, transfection of miR-146a mimics decreased IRAK2 expression in macrophages at both the protein and mRNA levels.}
{miR-34a overexpression in undifferentiated K562 cells reduced MYB protein by 74% and mRNA by 40% (Figure 4B).}
{miR-34a overexpression in undifferentiated K562 cells reduced MYB protein by 74% and mRNA by 40% (Figure 4B).}
{miR-34a overexpression in undifferentiated K562 cells reduced MYB protein by 74% and mRNA by 40% (Figure 4B).}
{B7-H3 mRNA level was not affected (data not shown).}
{miR-331-3p significantly downregulated expression of both ERBB-2 protein and RNA in each of the prostate cancer cell lines, independent of AR status (Figure 2A and 2B).}
{miR-331-3p significantly downregulated expression of both ERBB-2 protein and RNA in each of the prostate cancer cell lines, independent of AR status (Figure 2A and 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We clustered the DMSO and Matrigel datasets in parallel and identified five genes with the appropriate inverse expression pattern. Remarkably, the most prominently regulated gene of the five was Smad 3, which was represented on the microarray by three separate cDNAs, all of which revealed the same pattern of expression (Fig. 2B).}
{We then overexpressed miR-23a in the cardiomyocytes to test if endogenous MuRF1 is regulated by miR-23a. MuRF1 protein but not mRNA levels were significantly decreased in the presence of miR-23a (Fig. 5E).}
{The results showed that both the mRNA and the protein levels of BTG2 were elevated in HEp-2 cells transfected with miR-21 ASO compared with cells transfected with control ASO}
{A significant overexpression of miR-27b was observed in pre-miR-27b-transfected cells but not in pre-miR-negative control cells. Also, decreased levels of ST14 were observed (Fig. 3C), as shown by Western blotting as well as by QPCR analysis (Fig. 3D).}
{Despite significant decrease in Pten protein levels in TGF-Œ≤-treated MMC, no decrease in Pten mRNA levels was observed.}
{Despite significant decrease in Pten protein levels in TGF-Œ≤-treated MMC, no decrease in Pten mRNA levels was observed.}
{As shown in Figure 6C and 6D, KLF5 expression was upregulated by 2'OMe-miR-145 and was downregulated by pre-miR-145 at the protein level, but not at the mRNA level.}
{we examined the CCND1 mRNA by real time PCR and found that only miR-503 significantly reduced CCND1 mRNA.}
{"As shown in Figure 2, transfection with the miR-30a mimic caused a 25‚Äì40% decrease in beclin 1 mRNA (Fig. 2A), and a 25‚Äì60% decrease in beclin1 protein (Fig. 2B)."}
{We found a dose-dependent decrease of BLIMP-1 and XBP-1 in cells transfected with hsa-miR-127.}
{We found a dose-dependent decrease of BLIMP-1 and XBP-1 in cells transfected with hsa-miR-127.}
{Also, miR-31 reduced the endogenous mRNA levels of these six targets by two-fold in SUM-159 cells, as well as Fzd3, ITGA5, MMP16, RDX, and RhoA mRNA levels in 231 cells (Figure 4D).}
{Also, miR-31 reduced the endogenous mRNA levels of these six targets by two-fold in SUM-159 cells, as well as Fzd3, ITGA5, MMP16, RDX, and RhoA mRNA levels in 231 cells (Figure 4D).}
{Also, miR-31 reduced the endogenous mRNA levels of these six targets by two-fold in SUM-159 cells, as well as Fzd3, ITGA5, MMP16, RDX, and RhoA mRNA levels in 231 cells (Figure 4D).}
{Also, miR-31 reduced the endogenous mRNA levels of these six targets by two-fold in SUM-159 cells, as well as Fzd3, ITGA5, MMP16, RDX, and RhoA mRNA levels in 231 cells (Figure 4D).}
{Also, miR-31 reduced the endogenous mRNA levels of these six targets by two-fold in SUM-159 cells, as well as Fzd3, ITGA5, MMP16, RDX, and RhoA mRNA levels in 231 cells (Figure 4D).}
{In contrast, the mRNA levels of Cdk9 were not affected by overexpressing miR-1 (Figure 4B).}
{WT miR-1 significantly reduced the levels of Bcl-2 Mrna in cardiomyocytes in the absence and presence of H2O2.}
{This demonstrated that only in cells expressing miR-200c are the mRNA levels of TCF8 (ZEB1) clearly reduced.}
{The data showed comparable steady-state mRNA levels of uPA and c-met (Fig. 4A,B), providing evidence that miR-23b in SKHep1C3 cells can lead to decreased uPA and c-met protein expression without affecting the amounts of their mRNA.}
{The data showed comparable steady-state mRNA levels of uPA and c-met (Fig. 4A,B), providing evidence that miR-23b in SKHep1C3 cells can lead to decreased uPA and c-met protein expression without affecting the amounts of their mRNA.}
{The data showed comparable steady-state mRNA levels of uPA and c-met (Fig. 4A,B), providing evidence that miR-23b in SKHep1C3 cells can lead to decreased uPA and c-met protein expression without affecting the amounts of their mRNA.}
{The data showed comparable steady-state mRNA levels of uPA and c-met (Fig. 4A,B), providing evidence that miR-23b in SKHep1C3 cells can lead to decreased uPA and c-met protein expression without affecting the amounts of their mRNA.}
{The data showed comparable steady-state mRNA levels of uPA and c-met (Fig. 4A,B), providing evidence that miR-23b in SKHep1C3 cells can lead to decreased uPA and c-met protein expression without affecting the amounts of their mRNA.}
{The data showed comparable steady-state mRNA levels of uPA and c-met (Fig. 4A,B), providing evidence that miR-23b in SKHep1C3 cells can lead to decreased uPA and c-met protein expression without affecting the amounts of their mRNA.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR2 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR3 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR4 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR5 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR6 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR7 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR8 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{miR-129 targets FNDC3b, TP53INP1, ETV6, GALNT1, TNPO1, ZFP91, SCC-112, and BMPR9 were significantly down-regulated in non‚Äìmuscle-invasive tumors with later progression.}
{"As shown in Fig. 4B, fndc3b mRNA levels were not significantly affected, whereas protein levels decreased substantially after treatmentwith miR-143."}
{the level of Bmf mRNA detected by RT-PCR was not significantly changed (Fig.6 C).}
{the level of Bmf mRNA detected by RT-PCR was not significantly changed (Fig.6 C).}
{we confirmed that expression of the mRNAs for integrin subunits a5 (ITGA5) and av, S1P1, and MKK4 was reduced in response to miR-92a overexpression.}
{The levels of Dlx5 mRNA in cells transfected with miR-141 or -200a were  unchanged compared with BMP-2-stimulated cells examined by qRT-PCR using a real time-PCR (Fig. 4D, panel i) and semiquantitative RT-PCR (Fig. 4D, panel iii).}
{The levels of Dlx5 mRNA in cells transfected with miR-141 or -200a were  unchanged compared with BMP-2-stimulated cells examined by qRT-PCR using a real time-PCR (Fig. 4D, panel i) and semiquantitative RT-PCR (Fig. 4D, panel iii).}
{miR-195 overexpression caused a reduced mRNA level in CDK6 but not in cyclin D1 and E2F3.}
{miR-195 overexpression caused a reduced mRNA level in CDK6 but not in cyclin D1 and E2F3.}
{miR-195 overexpression caused a reduced mRNA level in CDK6 but not in cyclin D1 and E2F3.}
{miR-195 overexpression caused a reduced mRNA level in CDK6 but not in cyclin D1 and E2F3.}
{miR-195 overexpression caused a reduced mRNA level in CDK6 but not in cyclin D1 and E2F3.}
{In a contrary, both RT-PCR-based study and immunohistochemistrybased analysis of gene expression demonstrated that GCA mRNA is present in hMSC and regulated by miR-489 and -27a (Fig. 4).}
{In a contrary, both RT-PCR-based study and immunohistochemistrybased analysis of gene expression demonstrated that GCA mRNA is present in hMSC and regulated by miR-489 and -27a (Fig. 4).}
{"RT-PCR-based study of gene expression demonstrated that both CHRD and PEX7 mRNA are present inhMSC but only PEX7 is regulated by miR-489 and -27a (Fig. S6a)."}
{"RT-PCR-based study of gene expression demonstrated that both CHRD and PEX7 mRNA are present inhMSC but only PEX7 is regulated by miR-489 and -27a (Fig. S6a)."}
{Overexpression of either miR-221 or miR-222 resulted in significant (P < 0.05)significant effect on the Bax mRNA level .}
{Overexpression of either miR-221 or miR-222 resulted in significant (P < 0.05)significant effect on the Bax mRNA level .}
{"ALL-derived TOM-1 and NALM-20 cells nucleofected with pre-miR-124a showed an increase in expression of hsa-miR-124a (Fig. 2A) and a decrease in CDK6 mRNA and CDK6 and phosphorylated retinoblastoma (Rb-P) protein (Fig. 3B) levels in comparison with cells transfected with pre-miRscr ambledcontrol or empty vector."}
{qRTPCRs showed that p21 mRNA expression was diminished approximately 30% by the miR-93 mimic and 40% by the miR-106b mimic, vs. 94% by the control p21-siRNA (Figure 7A).}
{qRTPCRs showed that p21 mRNA expression was diminished approximately 30% by the miR-93 mimic and 40% by the miR-106b mimic, vs. 94% by the control p21-siRNA (Figure 7A).}
{Bim mRNA expression did not change following transfection of a miR-25 mimic.}
{miR-15a can reduce the translation of Slc12a2, Cldn12, and Bdnf mRNAs when each is coexpressed with this miRNA.}
{miR-15a can reduce the translation of Slc12a2, Cldn12, and Bdnf mRNAs when each is coexpressed with this miRNA.}
{miR-15a can reduce the translation of Slc12a2, Cldn12, and Bdnf mRNAs when each is coexpressed with this miRNA.}
{In addition, the level of FOXP3 was twofold lower in lenti-miR-31 transduced cells compared with lenti-miR-ctrl and non-transduced cells.}
{The corresponding levels of mRNA were also significantly reduced.}
{The corresponding levels of mRNA were also significantly reduced.}
{The corresponding levels of mRNA were also significantly reduced.}
{The corresponding levels of mRNA were also significantly reduced.}
{The corresponding levels of mRNA were also significantly reduced.}
{The corresponding levels of mRNA were also significantly reduced.}
{The corresponding levels of mRNA were also significantly reduced.}
{After 24- or 48-hr transfection, KRT7 mRNA expression was significantly repressed (p < 0.05) by miR-30a-3p, miR-133a and miR-199a* (Fig. 4b).}
{After 24- or 48-hr transfection, KRT7 mRNA expression was significantly repressed (p < 0.05) by miR-30a-3p, miR-133a and miR-199a* (Fig. 4b).}
{After 24- or 48-hr transfection, KRT7 mRNA expression was significantly repressed (p < 0.05) by miR-30a-3p, miR-133a and miR-199a* (Fig. 4b).}
{the mRNA expression levels of RTKN were reduced slightly, when compared to the vectoronly control (Fig. 3D).}
{MiR-449 overexpression (50 nmol/L) suppressed >70% WISP2 mRNA expression (Fig. 2B).}
{analysis by quantitative RT-PCR revealed that miR-302b was also capable of reducing the amount of p63 mRNA (Fig. 2C).}
{analysis by quantitative RT-PCR revealed that miR-302b was also capable of reducing the amount of p63 mRNA (Fig. 2C).}
{no significant change in HDAC4 and TGFŒ≤3 mRNA levels was found.}
{no significant change in HDAC4 and TGFŒ≤3 mRNA levels was found.}
{Col1a1 mRNA and protein were down-regulated in miR-29b overexpressing MC3T3 cells (Fig. 4B),}
{Luciferase assays (Fig. 4C) and decreased mRNA levels (Fig. 4D) also validated that miR-29b directly targets other collagen genes, including Col5a3, a minor component of bone tissue, and Col4a2, a basement membrane collagen.}
{Luciferase assays (Fig. 4C) and decreased mRNA levels (Fig. 4D) also validated that miR-29b directly targets other collagen genes, including Col5a3, a minor component of bone tissue, and Col4a2, a basement membrane collagen.}
{Increasing miR-196a levels in BIC-1 cells for 48 hours with the mimic resulted in 69%, 98%, and 20% decrease in S100A9, SPRR2C, and KRT5 mRNA levels.}
{Increasing miR-196a levels in BIC-1 cells for 48 hours with the mimic resulted in 69%, 98%, and 20% decrease in S100A9, SPRR2C, and KRT5 mRNA levels.}
{Increasing miR-196a levels in BIC-1 cells for 48 hours with the mimic resulted in 69%, 98%, and 20% decrease in S100A9, SPRR2C, and KRT5 mRNA levels.}
{RUNX3 mRNA expression in anti‚ÄìmiR-532-5p miRNA‚Äìtransfected melanoma cells was up-regulated relative to anti-miR negative control‚Äìtransfected melanoma cells (Fig. 4).}
{Induction of miR-605 reduced SEC24D mRNA and protein levels, while anti-miR-605 increased SEC2D mRNA and protein levels, confirming miR-605‚Äôs effect on endogenous SEC24D (Fig. 5).}
{NFATc2 mRNA levels (Figure 5B) were however unchanged between samples.}
{On the other hand, the levels of ERK5 mRNAs evaluated by qRTPCR were almost unchanged in the same samples.}
{transfection of miR-491 induced around 40% reduction in Bcl-XL mRNA levels (Fig. 3c).}
{As shown in Fig. 3, miR-497 inhibitor effectively increases (Fig. 3B), whereas miR-497 mimic decreases (Fig.3C) the expression of bcl-2 and bcl-w in mouse N2A cells subjected to 3 hours of OGD followed by 4 hours of recovery time. Of}
{Content of miR-696 did not significantly affect the expression of PGC-1  mRNA (Fig. 4B).}
{The results showed that the cells treated with the miR-133a mimic decreased NFATc4 mRNA levels 65% compared with cells treated with the control mimic (P   0.05) (Fig. 3A).}
{The results showed that the cells treated with the miR-133a mimic decreased NFATc4 mRNA levels 65% compared with cells treated with the control mimic (P   0.05) (Fig. 3A).}
{Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA (Figure 1d, mRNA).}
{Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA (Figure 1d, mRNA).}
{Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA (Figure 1d, mRNA).}
{Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA (Figure 1d, mRNA).}
{Introduction of the miRNAs resulted in downregulation of RECK protein (Figure 1d,Protein) with no appreciable changes in the level of RECK mRNA (Figure 1d, mRNA).}
{Transfection with (AS)miR-221 reduced miR-221 expression, and increased both the mRNA and protein levels of p85a (Fig. 5A,B).}
{overexpression of miR-33 resulted in reduced expression of ABCA1, but not ABCG1, mRNA (Fig. 2E,lanes 1‚Äì4), as well as reduced ABCA1 protein expression in these human hepatoma cells (Fig. 2F);}
{overexpression of miR-33 resulted in reduced expression of ABCA1, but not ABCG1, mRNA (Fig. 2E,lanes 1‚Äì4), as well as reduced ABCA1 protein expression in these human hepatoma cells (Fig. 2F);}
{overexpression of miR-33 resulted in reduced expression of ABCA1, but not ABCG1, mRNA (Fig. 2E,lanes 1‚Äì4), as well as reduced ABCA1 protein expression in these human hepatoma cells (Fig. 2F);}
{PANC-1 and MIAPaCa-2 cells were transfected with pre-miR-217, prescramble control, 217-vector or pcDNA 3.1 and the results showed that upregulation of miR-217 led to a dramatic reduction in KRAS expression at the protein level (Figure 4E and F, Supplementary Figure 1C is available at Carcinogenesis Online) but not at mRNA level}
{Both Suv39h1 mRNA levels (Fig. 3A) and protein levels (Fig. 3B) were significantly decreased in db/  cells toward that seen in db/db cells after transfection with the miR-125b relative to NC-M.}
{"In murine 70Z/3 cells, we observed a similar repression of Foxp1 at the protein level within 4 days of transduction (Figure 3E). Analysis of Foxp1 RNA in B cell subsets showed an inverse correlation with miR-34a amounts at the pro- and pre-B cell stages (Figure 3F; compare with Figure2C). Having observed repression of Foxp1 in cell lines, we also examined Foxp1 mRNA expression in whole bone marrow from miR-34a mice. Foxp1 mRNA is significantly downregulatedin the bone marrow of mice transduced with miR-34a ("}
{Notably, real-time PCR demonstrated that CUGBP2 messenger RNA copy numbers were similar among these groups (data not shown).}
{Notably, real-time PCR demonstrated that CUGBP2 messenger RNA copy numbers were similar among these groups (data not shown).}
{Expression of three out of the four putative target genes were significantly decreased in miR-206 over expressed cells suggesting that these three genes are true targets of miR-206.}
{Expression of three out of the four putative target genes were significantly decreased in miR-206 over expressed cells suggesting that these three genes are true targets of miR-206.}
{Expression of three out of the four putative target genes were significantly decreased in miR-206 over expressed cells suggesting that these three genes are true targets of miR-206.}
{Overexpression of miR-21 had no significant effect on Faslg mRNA after OGD compared to miR-67 negative control}
{"There was no significant differencein TP53 mRNA levels after miR-380-5p overexpression"}
{miR-155 has no effect on the mRNA expression level of MyD88. In contrast, overexpression of miR-155 mimics decreased MyD88 protein content in a dose and time-dependent manner (Fig. 2B and C). }
{Overexpression of miR-17 significantly reduced several predicted targets, including the cell cycle inhibitor p21, the S1P receptor EDG1, and the protein kinase Janus kinase 1 }
{In agreement with this finding, macrophages transfected with pre-let-7a had reduced levels of endogenous Œ∫B-Ras2, while overexpression of pre-miR-125b led to enhanced Œ∫B-Ras2 expression (Figure 6D). }
{In agreement with this finding, macrophages transfected with pre-let-7a had reduced levels of endogenous Œ∫B-Ras2, while overexpression of pre-miR-125b led to enhanced Œ∫B-Ras2 expression (Figure 6D). }
{Western blot analysis showed that transfection of miR-1 significantly decreased the expression level of endogenous Pim-1 protein (Fig. 5A & B). Additionally, there was no significant decrease in the mRNA level of Pim-1 upon miR-1 transfection}
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{When we selected all miR-31 predicted targets (TargetScan, Release 4.0) from the mRNA microarray data, we found that all of them were upregulated in CAFs when miR-31 was downregulated (Fig. 4A). }
{we transfected MGC-803 cells with miR-148b mimics and the NC. Forty-eight hours after transfection, we examined the CCKBR protein levels in cells by western blot. Obviously, CCKBR protein levels were suppressed by miR-148b mimics in MGC-803 cells (Figure ‚Äã(Figure4C).4C). Despite the effect of miR-148b on CCKBR protein levels, no effect on the CCKBR mRNA level was detected by qRT-PCR (Figure ‚Äã(Figure4D4D).}
{In a parallel experiment, we monitored transcript levels of EGFR and IRS-2 by qRT-PCR reactions normalized to levels of GAPDH mRNA (Supplementary Fig. 3B) and found a significant decrease of both EGFR and IRS-2 mRNA levels resulting from increased expression of miR-7.}
{In a parallel experiment, we monitored transcript levels of EGFR and IRS-2 by qRT-PCR reactions normalized to levels of GAPDH mRNA (Supplementary Fig. 3B) and found a significant decrease of both EGFR and IRS-2 mRNA levels resulting from increased expression of miR-7.}
{We found that miR-7 transfection decreased both mRNA (data not shown) and protein levels (Fig. 4F) of Ack1 compared to GAPDH mRNA and actin in both cell types.}
{As a result, miR-27a decreased TRŒ≤1 protein levels without affecting TRŒ≤1 mRNA levels in NRVMs, and the miR-27a decoy increased TRŒ≤1 protein levels (Fig. 5A and B). }
{Transfection of Hepa1‚Äì6 cells with the miR-483-5p overexpression or knockdown plasmid resulted in a significant decrease or increase, respectively, in the amount of mRNA expressed from the Socs3 gene (Fig. 5). }
{The overexpression and knockdown plasmids had an inverse effect on the expression of Tnf-Œ±. }
{As shown in Fig. 7D, an increase of SFRS1 mRNA in anti-miR-10a-transfected cells occurred, as compared with negative control anti-miR}
{As shown in Fig. 7D, an increase of SFRS1 mRNA in anti-miR-10a-transfected cells occurred, as compared with negative control anti-miR}
{Forced miR-200b expression decreased Flt1 mRNA and VEGFR1 protein levels by 73% and 38%, respectively (Fig. 1C), }
{To determine whether miR-155 targeted AT1R mRNA for degradation, real-time RT-PCR demonstrated that AT1R mRNA levels remained unchanged following miR-155 transfection (Fig. 2B). However, western blot assay revealed significantly reduced AT1R protein expression in AFs transfected with pSUPER/miR-155 compared with controls (Fig. 2C). }
{Expression of endogenous TBP in mRNA as well as protein level was decreased in STHdhQ111/HdhQ111 cells expressing exogenous miR-146a (Fig. 4B and C). }
{To determine whether miR-214 specifically attenuates N-ras expression, we measured the endogenous N-ras mRNA levels by qPCR after transfection of 214in or 214mi in C2C12 cells. We found that inhibition of miR-214 expression with 214in increased whereas enhancing miR-214 expression with 214mi decreased N-ras mRNA levels relative to that in the control cells transfected with a nonspecific miRNA (Fig. 5A).}
{in contrast, when the prediction algorithms miRanda and RNAhybrid were applied, the same 4 target genes (Nqo1, Pdpn, CXCL3, and Rad23b) (Table ‚Äã(Table1)1) demonstrated a persistent downregulated status at 1, 3, 7, and 14 d (Figure ‚Äã(Figure3).3). The miRNA array and the microarray data have been deposited in the Gene Expression Omnibus (accession number [GEO: {"type":"entrez-geo","attrs":{"text":"GSE21423","term_id":"21423"}}GSE21423]).}
{in contrast, when the prediction algorithms miRanda and RNAhybrid were applied, the same 4 target genes (Nqo1, Pdpn, CXCL3, and Rad23b) (Table ‚Äã(Table1)1) demonstrated a persistent downregulated status at 1, 3, 7, and 14 d (Figure ‚Äã(Figure3).3). The miRNA array and the microarray data have been deposited in the Gene Expression Omnibus (accession number [GEO: {"type":"entrez-geo","attrs":{"text":"GSE21423","term_id":"21423"}}GSE21423]).}
{in contrast, when the prediction algorithms miRanda and RNAhybrid were applied, the same 4 target genes (Nqo1, Pdpn, CXCL3, and Rad23b) (Table ‚Äã(Table1)1) demonstrated a persistent downregulated status at 1, 3, 7, and 14 d (Figure ‚Äã(Figure3).3). The miRNA array and the microarray data have been deposited in the Gene Expression Omnibus (accession number [GEO: {"type":"entrez-geo","attrs":{"text":"GSE21423","term_id":"21423"}}GSE21423]).}
{in contrast, when the prediction algorithms miRanda and RNAhybrid were applied, the same 4 target genes (Nqo1, Pdpn, CXCL3, and Rad23b) (Table ‚Äã(Table1)1) demonstrated a persistent downregulated status at 1, 3, 7, and 14 d (Figure ‚Äã(Figure3).3). The miRNA array and the microarray data have been deposited in the Gene Expression Omnibus (accession number [GEO: {"type":"entrez-geo","attrs":{"text":"GSE21423","term_id":"21423"}}GSE21423]).}
{RNA isolated from transfected C2BBe1 cells was assayed for hAT1R mRNA levels. These results demonstrated that transfection with miR-802 did not significantly decrease hAT1R steady-state mRNA levels in these cells }
{However, results from our real-time PCR and western blot analysis revealed that with treatment of miR-23b mimics (150 pmol in 24-well plate) in BRL-3A cells, Smad3 expression notably decreased in both mRNA and protein level; }
{First, we demonstrated that overexpression of miR-100 represses mTOR expression on both the mRNA and protein levels in endothelial cells, whereas miR-100 inhibition resulted in a modest but significant upregulation of mTOR }
{Transfection of the pre-miR-3960, rather than the control, resulted in a decrease in the Hoxa2 protein levels after 48 h (Fig. 4C). However, the Hoxa2 mRNA levels were not affected (Fig. 4D). }
{ Indeed, miR-93 and miR-106b expression efficiently decreased both Tgfbr2 and p21 protein levels (Figure 5A and D) and p21 mRNA levels were decreased by ~25‚Äì30% while Tgfbr2 was decreased by ~60‚Äì70% }
{ Indeed, miR-93 and miR-106b expression efficiently decreased both Tgfbr2 and p21 protein levels (Figure 5A and D) and p21 mRNA levels were decreased by ~25‚Äì30% while Tgfbr2 was decreased by ~60‚Äì70% }
{ Indeed, miR-93 and miR-106b expression efficiently decreased both Tgfbr2 and p21 protein levels (Figure 5A and D) and p21 mRNA levels were decreased by ~25‚Äì30% while Tgfbr2 was decreased by ~60‚Äì70% }
{ Indeed, miR-93 and miR-106b expression efficiently decreased both Tgfbr2 and p21 protein levels (Figure 5A and D) and p21 mRNA levels were decreased by ~25‚Äì30% while Tgfbr2 was decreased by ~60‚Äì70% }
{To further confirm that miR-9 affects FoxP1 expression at a protein level, miR-9-1 and miR-9-2 were co-transfected with FoxP1 cDNA sequences containing both the coding region and the 3‚Ä≤-UTR in Neuro2A cells. MiR-9-1 and miR-9-2, but not miR-9-Mut, significantly reduced FoxP1 protein but not FoxP1 mRNA }
{In contrast, CD44 mRNA (Supplementary Fig. 4e) and protein (Supplementary Fig. 11c) were increased in anti-34a transfected tumors. }
{In contrast, CD44 mRNA (Supplementary Fig. 4e) and protein (Supplementary Fig. 11c) were increased in anti-34a transfected tumors. }
{Thus, overexpressing mir-200c and mir-141 in the PC-3 cells, or mir-141 alone, produced a 60% and 30% decrease in the JAG1 protein, respectively (Figure 4A, upper blot), without significantly altering JAG1 mRNA levels }
{Thus, overexpressing mir-200c and mir-141 in the PC-3 cells, or mir-141 alone, produced a 60% and 30% decrease in the JAG1 protein, respectively (Figure 4A, upper blot), without significantly altering JAG1 mRNA levels }
{To determine whether miR-214 specifically attenuates N-ras expression, we measured the endogenous N-ras mRNA levels by qPCR after transfection of 214in or 214mi in C2C12 cells. We found that inhibition of miR-214 expression with 214in increased whereas enhancing miR-214 expression with 214mi decreased N-ras mRNA levels relative to that in the control cells transfected with a nonspecific miRNA (Fig. 5A).}
{To determine whether miR-214 specifically attenuates N-ras expression, we measured the endogenous N-ras mRNA levels by qPCR after transfection of 214in or 214mi in C2C12 cells. We found that inhibition of miR-214 expression with 214in increased whereas enhancing miR-214 expression with 214mi decreased N-ras mRNA levels relative to that in the control cells transfected with a nonspecific miRNA (Fig. 5A).}
{"As shown by qRT-PCR and immunocytochemistry, overexpression of mature hsa-miR-381 in U251/LRRC4+ cells resulted in the down-regulation of LRRC4 at the mRNA transcriptional (Fig. 4C) and posttranscriptional levels (Fig. 4D)."}
{"Overexpressionof miR-375 in AGS and MGC-803 cells greatlyreduced the protein level of JAK2, whereas the level ofJAK2 mRNA was not significantly affected (Figure 4Band Supplementary information, Figure S4)"}
{"Overexpressionof miR-375 in AGS and MGC-803 cells greatlyreduced the protein level of JAK2, whereas the level ofJAK2 mRNA was not significantly affected (Figure 4Band Supplementary information, Figure S4)"}
{"E2F3 protein expression was significantly decreased inT24 and 5637 cells after transfection with miR-125b (Fig.8b), whereas the E2F3 mRNA was almost unchanged (Fig.8a), which suggested that miR-125b may regulate the level ofE2F3 protein at the post-transcriptional level but not themRNA level."}
{"Overexpressionof miR-448 reduced the protein level of KLF5, whereas itdid not change the Klf5 mRNA level (Fig. 4C and SupplementalFig. 3B)."}
{"Transfection of miR-27 in Sol8 cellsdecreased Mef2c expression by ~40% (Figure 6B) while inhibition of miR-27b leads to a4-fold increase in Mef2c transcript expression."}
{"To assess the influence of miR-184, BIN3mRNA expression in the cell lines was assayed, andwas not significantly different between both cell lines(Table 4)."}
{"The expressionlevels of differentially expressed genes between LoVo andNCM460 cell lines were analysed by the statistical analysis with aP-value of  0.05. A total of 583 differentially expressed geneswith 2-fold or more changes in the expression intensity betweenthe two cell lines were selected for further analysis (Table S2). Tofurther validate the true gene targets of miR-26b, four genes(TAF12, PTP4A1, CHFR and ALS2CR2) among the differentiallyexpressed genes between LoVo and NCM460 cell lines, were alsopredicted by the miRNA targets by TargetScan, PicTar andmiRanda (Fig. 8)."}
{"The expressionlevels of differentially expressed genes between LoVo andNCM460 cell lines were analysed by the statistical analysis with aP-value of  0.05. A total of 583 differentially expressed geneswith 2-fold or more changes in the expression intensity betweenthe two cell lines were selected for further analysis (Table S2). Tofurther validate the true gene targets of miR-26b, four genes(TAF12, PTP4A1, CHFR and ALS2CR2) among the differentiallyexpressed genes between LoVo and NCM460 cell lines, were alsopredicted by the miRNA targets by TargetScan, PicTar andmiRanda (Fig. 8)."}
{"The expressionlevels of differentially expressed genes between LoVo andNCM460 cell lines were analysed by the statistical analysis with aP-value of  0.05. A total of 583 differentially expressed geneswith 2-fold or more changes in the expression intensity betweenthe two cell lines were selected for further analysis (Table S2). Tofurther validate the true gene targets of miR-26b, four genes(TAF12, PTP4A1, CHFR and ALS2CR2) among the differentiallyexpressed genes between LoVo and NCM460 cell lines, were alsopredicted by the miRNA targets by TargetScan, PicTar andmiRanda (Fig. 8)."}
{"The expressionlevels of differentially expressed genes between LoVo andNCM460 cell lines were analysed by the statistical analysis with aP-value of  0.05. A total of 583 differentially expressed geneswith 2-fold or more changes in the expression intensity betweenthe two cell lines were selected for further analysis (Table S2). Tofurther validate the true gene targets of miR-26b, four genes(TAF12, PTP4A1, CHFR and ALS2CR2) among the differentiallyexpressed genes between LoVo and NCM460 cell lines, were alsopredicted by the miRNA targets by TargetScan, PicTar andmiRanda (Fig. 8)."}
{MOR expression was determined by western blotting. When SH-SY5Y cells were transfected with increasing amounts of the LNA-let-7 inhibitor, MOR expression was up-regulated in an antisense dose-dependent fashion (Fig. 2).}
{We confirmed these results using a mouse kidney cell line, TCMK-1 cells. Ybx1 protein levels were decreased by over 80% by the miR-216a mimic, whereas Ybx1 mRNA levels were not altered }
{"The levels of RB1 mRNAand protein in the anti-miR-106a group were both above thelevels seen in the NC inhibitor groups. In contrast, the levels ofRB1 mRNA and protein in the miR-106a mimic group wereboth below the levels seen in the NC mimic group (Figs. 7Cand D)."}
{"As shown in Fig. 2A and 2B, transfection with miR-101 mimicdid not significantly change the mRNA level of MKP-1 as com-pared with control dsRNA. We also have analyzed the effect ofmiR-101 on the protein level of MKP-1 using Western blot analyses.The results reveal that transfection of miR-101 mimic but notcontrol dsRNA markedly inhibits the production of MKP-1 protein(Fig. 2C). These results suggest that miR-101 may function at thetranslational level."}
{In addition, real time PCR and western blot analysis revealed that the expression of RB1 mRNA and protein was impaired by the treatment with miR-192 mimics in A549 cells (Figure 3C and D). }
{Semi-quantitative analysis of western blot data showed a significant inhibition of NOBOX expression in the miR-196a-transfected cells }
{To directly examine the regulation of Abcc3 by mmu-miR-665, RAW 264.7 cells were transfected with vehicle, or a mmu-miR-665 precursor, or a control miRNA precursor. As shown in Figure 3A and B, mmu-miR-665 significantly inhibited Abcc3 expression at both mRNA and protein levels as assessed by qRT-PCR and Western blotting, }
{Furthermore, the overexpression of miR-29a was able to markedly downregulate the expression of endogenous PTEN at the levels of mRNA and protein in HepG2 or MHCC-97L cells. }
{Furthermore, the overexpression of miR-29a was able to markedly downregulate the expression of endogenous PTEN at the levels of mRNA and protein in HepG2 or MHCC-97L cells. }
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{To determine whether these miRNAs affect endogenous Runx2 expression in distinct cell types, we transfected these miRNAs into MC3T3-E1 osteoblasts and ATDC5 chondrocytes and examined Runx2 mRNA and protein levels. Except for miR-30c in MC3T3 and miR-133a in ATDC5 cells, these miRNAs repress Runx2 expression at the protein level but not the mRNA level (Fig. S3).}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{Overexpression of miR-124 produced a statistically significant decrease in the endogenous Mct1 mRNA level. This confirms that miR-124 is able to target naturally occurring Mct1 mRNA and that this results in mRNA degradation. Although the results for miR-29a and -29b fell below the level of statistical significance, the pattern of effects observed in the luciferase assay (Fig. 3A and B) were broadly replicated. miR-29a and miR-29b thus both tended to cause decreases in Mct1 mRNA levels, with miR-29a exerting a larger effect than miR-29b. This suggests that miR-29a and miR-29b may target Mct1 at least partially through mRNA degradation.}
{qRT-PCR and westernblot analysis revealed that miR-34a drastically inhibited the expression of INHBB and Met on both mRNA and protein levels (Figure 3A,B). }
{" In addition, col2a1 expression was found repressed significantly if miR-29a/b mimics were transiently transfected to the chondrocytes, demonstrated by RT-PCR (Fig. 6A). The repression on protein level was further confirmed by immunostaining (Fig. 6B) and western blotting (Fig. 6C). Therefore, it was concluded that miR-29a/b directly targeted 3‚Ä≤ UTR of col2a1 to repress its expression."}
{"In addition, col2a1 expression was found repressed significantly if miR-29a/b mimics were transiently transfected to the chondrocytes, demonstrated by RT-PCR (Fig. 6A). The repression on protein level was further confirmed by immunostaining (Fig. 6B) and western blotting (Fig. 6C). Therefore, it was concluded that miR-29a/b directly targeted 3‚Ä≤ UTR of col2a1 to repress its expression."}
{Consistently, miR-1 transgenic hearts showed significantly reduced Cdc42 mRNA and protein levels (Fig. 5, E and F), suggesting a repressive relationship between miR-1 and Cdc42 in vivo.}
{We tested if miR-485 controlled SV2A expression in hippocampal neurons by miR-485 overexpression and inhibition. miR-485 overexpression decreased both transcript abundance (n = 3; P < 0.05) (Fig. 2B) and protein expression (Fig. 2C) of SV2A relative to both an untreated control and negative controls for the miR-M and miR-I containing random sequences validated to not affect miR function. }
{A single-stranded oligonucleotide designed to bind miR-23a (anti‚ÄìmiR-23a) was used to inhibit miR-23a binding to its target mRNA. Inhibition of miR-23a by anti‚ÄìmiR-23a led to a significant increase in XIAP mRNA expression (Fig. 4A, bars 1 and 2 vs. bar 3; P < 0.05). Scrambled anti-miRNA had no effect on XIAP mRNA expression (Fig. 4A, bar 1 vs. bar 2; P > 0.05).}
{The inhibitory role of miR-146a on Notch1 is mainly through posttranscriptional control since it does not change the mRNA level of Notch1 (Fig. 5E). }
{Overexpression of miR-206 in normoxic conditions significantly reduced TIMP-3 mRNA (Figure 9A) and protein levels (Figure 9B). }
{"In order to validate whether miR-19b is capable of regulating NeuroD1 expression, we cloned the DNA sequence corresponding to the entire NeuroD1 mRNA into pEGFP-C1 to construct EGFP-NeuroD1 fusion protein expression vector (pEGFP-C1-NeuroD1), then the vector was co-transfected with either synthesized miR-19b or miR-19b inhibitor into 3T3 cells. The overexpression of miR-19b was confirmed by qRT-PCR (Fig. 3A). Also, qRT-PCR results showed that overexpression of miR-19b decreased NeuroD1 mRNA level (Fig. 3B). Western blotting results showed that the NeuroD1 protein was significantly inhibited by miR-19b (Fig. 3D). Meanwhile, the expression of EGFP protein was repressed because of the reducing NeuroD1 (Fig. 3C). Similar results were observed in 293GP cells which were co-transfected with pEGFP-C1-NeuroD1, miR-19b and/or miR-19b inhibitor (Fig. S3)."}
{"Lenti.miR-503reduced cdc25A and CCNE1 at mRNA and protein level inHUVECs in comparison with GFP-HUVECs."}
{"Lenti.miR-503reduced cdc25A and CCNE1 at mRNA and protein level inHUVECs in comparison with GFP-HUVECs."}
{"Lenti.miR-503reduced cdc25A and CCNE1 at mRNA and protein level inHUVECs in comparison with GFP-HUVECs."}
{"H1299, MDA-MB-231, HCT116 and Rkocells were transfected with control-miR, miR-34a ormiR-199a. As miR-199a and miR-199b have similarseed sequences and binds with more or less equal freeenergy to the Axl 30-UTR, miR-199a was used forfurther transfection experiments. qRT‚ÄìPCR resultsshowed that both the miRs (miR-34a and miR-199a)significantly reduced Axl-transcript levels (Figure 2b).Furthermore, western blot analysis confirmed the downregulationof Axl protein amounts (Figure 2c)."}
{"H1299, MDA-MB-231, HCT116 and Rkocells were transfected with control-miR, miR-34a ormiR-199a. As miR-199a and miR-199b have similarseed sequences and binds with more or less equal freeenergy to the Axl 30-UTR, miR-199a was used forfurther transfection experiments. qRT‚ÄìPCR resultsshowed that both the miRs (miR-34a and miR-199a)significantly reduced Axl-transcript levels (Figure 2b).Furthermore, western blot analysis confirmed the downregulationof Axl protein amounts (Figure 2c)."}
{"To determine if the mmu-miR-466h inhibition indepleted media affected the expression of bcl2l2, birc6,dad1, stat5a, and smo genes, their mRNA levels werecompared in depleted media in the presence or the absenceof anti-miR-466h. The mRNA level for each gene increasedbetween 4- and 23-fold in the presence of anti-miR-466hwith the greatest relative increases observed in smo and dad1genes (Fig. 5B). Addition of the irrelevant anti-miR as anegative control at the same concentration as anti-miR-466hto the depleted media generated the respective mRNA levelsthat were comparable to their levels without inhibitor (datanot shown)."}
{"To determine if the mmu-miR-466h inhibition indepleted media affected the expression of bcl2l2, birc6,dad1, stat5a, and smo genes, their mRNA levels werecompared in depleted media in the presence or the absenceof anti-miR-466h. The mRNA level for each gene increasedbetween 4- and 23-fold in the presence of anti-miR-466hwith the greatest relative increases observed in smo and dad1genes (Fig. 5B). Addition of the irrelevant anti-miR as anegative control at the same concentration as anti-miR-466hto the depleted media generated the respective mRNA levelsthat were comparable to their levels without inhibitor (datanot shown)."}
{"To determine if the mmu-miR-466h inhibition indepleted media affected the expression of bcl2l2, birc6,dad1, stat5a, and smo genes, their mRNA levels werecompared in depleted media in the presence or the absenceof anti-miR-466h. The mRNA level for each gene increasedbetween 4- and 23-fold in the presence of anti-miR-466hwith the greatest relative increases observed in smo and dad1genes (Fig. 5B). Addition of the irrelevant anti-miR as anegative control at the same concentration as anti-miR-466hto the depleted media generated the respective mRNA levelsthat were comparable to their levels without inhibitor (datanot shown)."}
{"To determine if the mmu-miR-466h inhibition indepleted media affected the expression of bcl2l2, birc6,dad1, stat5a, and smo genes, their mRNA levels werecompared in depleted media in the presence or the absenceof anti-miR-466h. The mRNA level for each gene increasedbetween 4- and 23-fold in the presence of anti-miR-466hwith the greatest relative increases observed in smo and dad1genes (Fig. 5B). Addition of the irrelevant anti-miR as anegative control at the same concentration as anti-miR-466hto the depleted media generated the respective mRNA levelsthat were comparable to their levels without inhibitor (datanot shown)."}
{"To determine if the mmu-miR-466h inhibition indepleted media affected the expression of bcl2l2, birc6,dad1, stat5a, and smo genes, their mRNA levels werecompared in depleted media in the presence or the absenceof anti-miR-466h. The mRNA level for each gene increasedbetween 4- and 23-fold in the presence of anti-miR-466hwith the greatest relative increases observed in smo and dad1genes (Fig. 5B). Addition of the irrelevant anti-miR as anegative control at the same concentration as anti-miR-466hto the depleted media generated the respective mRNA levelsthat were comparable to their levels without inhibitor (datanot shown)."}
{"To confirm that miR-132 and miR-212 are responsible for the decrease inp250RhoGAP, we electroporated cellswith an anti-miR. Introduction of antimiRsto either miR-132 or miR-212 didnot prevent the down-regulation ofp250RhoGAP (data not shown) so wedesigned a degenerate anti-miR to blockboth miR-132 and miR-212 usinglocked nucleic acids. This dual anti-miRprevented the GnRH-induced decreasein p250RhoGAP mRNA compared with a scrambled control(Fig. 3E) showing that miR-132 and miR-212 are requiredfor down-regulation."}
{"To confirm that miR-132 and miR-212 are responsible for the decrease inp250RhoGAP, we electroporated cellswith an anti-miR. Introduction of antimiRsto either miR-132 or miR-212 didnot prevent the down-regulation ofp250RhoGAP (data not shown) so wedesigned a degenerate anti-miR to blockboth miR-132 and miR-212 usinglocked nucleic acids. This dual anti-miRprevented the GnRH-induced decreasein p250RhoGAP mRNA compared with a scrambled control(Fig. 3E) showing that miR-132 and miR-212 are requiredfor down-regulation."}
{"we determinedthe mRNA and protein levels of STAT3 in hASCs overexpressingmiR-21 or cells transfected with a miR-21-specificinhibitor. Real-time PCR and Western blot analyses showedthat miR-21-over-expressing hASCs exhibited less total andphospho-STAT3 expression and that anti-miR-21-transfectedhASCs exhibited increased STAT3 expression (Fig. 4C,D)."}
{"The fact that c-Fos protein was increased toa greater extent than c-Fos mRNA (25-fold versus 2- to 3-fold)suggested that miR155 represses c-Fos expression mainly at thelevel of translation."}
{"The fact that c-Fos protein was increased toa greater extent than c-Fos mRNA (25-fold versus 2- to 3-fold)suggested that miR155 represses c-Fos expression mainly at thelevel of translation."}
{"The results showed that miR-126-3p inhibitorcould promote effectively endogenic miR-126-3pincreased by qRT-PCR (Fig. 4a P\0.01). However, PgrmRNA levels were not altered compared to control(Fig. 4b P[0.05). Meanwhile, we examined protein levelsof PGR in MMECs after miR-126-3p mimics, inhibitor,or control into cells. As showed in Fig. 5, transfection ofmiR-126-3p mimics led to a significant down-regulation ofPGR protein (P\0.05). Alternatively, transfection ofmiR-126-3p inhibitor increased PGR protein levels comparedto control-transfected cells (P\0.05)."}
{"The results showed that miR-126-3p inhibitorcould promote effectively endogenic miR-126-3pincreased by qRT-PCR (Fig. 4a P\0.01). However, PgrmRNA levels were not altered compared to control(Fig. 4b P[0.05). Meanwhile, we examined protein levelsof PGR in MMECs after miR-126-3p mimics, inhibitor,or control into cells. As showed in Fig. 5, transfection ofmiR-126-3p mimics led to a significant down-regulation ofPGR protein (P\0.05). Alternatively, transfection ofmiR-126-3p inhibitor increased PGR protein levels comparedto control-transfected cells (P\0.05)."}
{"Western blot and reverse transcription(RT)‚ÄìPCR demonstrated that overexpression of miR-342dramatically suppressed endogenous DNMT1 both at protein andmRNA levels compared with negative control miRNA (Figure 2B)."}
{"To further confirm the interaction betweenmiR-140 and Dnpep, we coinjected a miR-140 duplex andDnpep mRNA into zebrafish embryos. Injection of miR-140causes defects in palatal skeletogenesis in zebrafish (9). Coinjectionof mouse Dnpep mRNA significantly reduced the occurrenceof the miR-140-induced palatal defect (Fig. 7A). Interestingly,coinjection of rat Dnpep mRNA also had the sameeffect. Zebrafish Dnpep lacks strongly predicted miR-140 bindingsites, and expression of endogenous zebrafish Dnpep wasunchanged 1 and 3 days after miR-140 injection (data notshown), suggesting that miR-140 does not regulate zebrafishDnpep;"}
{"To further confirm the interaction betweenmiR-140 and Dnpep, we coinjected a miR-140 duplex andDnpep mRNA into zebrafish embryos. Injection of miR-140causes defects in palatal skeletogenesis in zebrafish (9). Coinjectionof mouse Dnpep mRNA significantly reduced the occurrenceof the miR-140-induced palatal defect (Fig. 7A). Interestingly,coinjection of rat Dnpep mRNA also had the sameeffect. Zebrafish Dnpep lacks strongly predicted miR-140 bindingsites, and expression of endogenous zebrafish Dnpep wasunchanged 1 and 3 days after miR-140 injection (data notshown), suggesting that miR-140 does not regulate zebrafishDnpep;"}
{"Enhanced miR-296-5p expression resulted in amarked decrease of PUMA cellular mRNA and protein levels( Fig. 2B, C )."}
{"Enhanced miR-296-5p expression resulted in amarked decrease of PUMA cellular mRNA and protein levels( Fig. 2B, C )."}
{"The gene encoding caveolin-1 (Cav1), a key componentof caveolae and a mediator of insulin signalling, was among the miR-103/107 seed-containing genes that were downregulated after overexpressionof miR-107 in the liver, and upregulated after its silencing"}
{"To analyze expression of mir-378 and the IFNGR1 gene atdifferent luteal stages, real-time RT-PCR was carried out atfour luteal stages. The results revealed that mir-378 wasmore highly expressed in the mid- and late stages than inthe early and regressed stages (P<0.05), with the highestlevel being detected in the late stage and the lowest levelbeing detected in the early stage of CL (Fig. 2). TheIFNGR1 gene showed the lowest expression level in theearly stage of CL (P<0.05). Although expression of theIFNGR1 gene increased from mid- to the regressed stage(Fig. 3), it did not reach statistical significance."}
{"To determine if miR-124 affects ROCK2 and EZH2 expression in the HCC intracellular environment, we analysed the changes of ROCK2 and EZH2 expression in HCC cell line LM9 after miR-124 overexpression. Using real-time-PCR, wefound that the mRNA levels of both ROCK2 and EZH2 were dramatically reduced in miR-124 overexpressing LM9 and HepG2 cells"}
{"To determine if miR-124 affects ROCK2 and EZH2 expression in the HCC intracellular environment, we analysed the changes of ROCK2 and EZH2 expression in HCC cell line LM9 after miR-124 overexpression. Using real-time-PCR, wefound that the mRNA levels of both ROCK2 and EZH2 were dramatically reduced in miR-124 overexpressing LM9 and HepG2 cells"}
{"Wefound that the expression levels of Trp53inp1 mRNAs increasedafter inducing apoptosis by IL-3 withdrawal but that those ofTrp53inp1 mRNAs were repressed in miR-125b-transduced32Dcl3 cells compared with mock-transduced 32Dcl3 cells ateach time point. In addition, the numbers of apoptotic cellsdecreased in miR-125b-transduced cells but not in miR-30a,"}
{However, qRT-PCR analysis showed no significant change in Sox9 mRNA level in both transfected cells (Figure 3B-). Thus, these data demonstrate miR-145 inhibits Sox9 protein expression but not mRNA levels in mesenchymal stem cell line at early stage of chondrogenic differentiation.}
{ Likewise, in anti-miR-144 transfected HeLa and 3T3L1 cells, the relative expression of miR-144 was reduced to 0.019¬±0.09 and 0.033¬±0.11 respectively while a significant increase in IRS1 mRNA level was observed (HeLa: 5.607¬±0.217; 3T3L1 Regulation of IRS1 by miR-144 was further verified by immunocytochemistry and complementarily, the IRS1 protein expression correlated to that of the gene expression studies.}
{Ischemic progenitor cells were delivered with miR-124a mimics and incubated in the growth medium for 3 days. JAG1 and Notch intracellular domain (NICD) were assayed by real-time RT-PCR and Western blot. Compared with the miRNA mimic control, nanoparticle-delivered mature miR-124a resulted in a substantial decrease of JAG1 transcript and protein (Fig. 5F and G). }
{To confirm that Arpc3 is a genuine target of miR-29a/b, mouse N2a cells were transfected with pEZX plasmid expression clones for miR-29a or -29b (see Effect of candidate miRs on synaptic structure and function). The coexpression of GFP from the pEZX vector enabled selection of miR-29a‚Äì or -29b‚Äìoverexpressing cells only. As demonstrated in Fig. 6 B, the Arpc3 transcript was significantly down-regulated by both miR-29a and -29b (27 ¬± 9%, P = 0.048; 42 ¬± 4%, P = 0.0003; n = 3; Fig. 6 B). }
{To confirm that Arpc3 is a genuine target of miR-29a/b, mouse N2a cells were transfected with pEZX plasmid expression clones for miR-29a or -29b (see Effect of candidate miRs on synaptic structure and function). The coexpression of GFP from the pEZX vector enabled selection of miR-29a‚Äì or -29b‚Äìoverexpressing cells only. As demonstrated in Fig. 6 B, the Arpc3 transcript was significantly down-regulated by both miR-29a and -29b (27 ¬± 9%, P = 0.048; 42 ¬± 4%, P = 0.0003; n = 3; Fig. 6 B). }
{"We also examined expression of survivin mRNA in 12 pairs of human tissue samples from Fig. 1B to determinewhether there was an inverse relationship between survivinand miR-708 expression."}
{"We also examined expression of survivin mRNA in 12 pairs of human tissue samples from Fig. 1B to determinewhether there was an inverse relationship between survivinand miR-708 expression."}
{"We also examined expression of survivin mRNA in 12 pairs of human tissue samples from Fig. 1B to determinewhether there was an inverse relationship between survivinand miR-708 expression."}
{"Furthermore, endogenousCAMTA1 mRNA as well as protein levels wereelevated, when miR-9 or miR-9* was inhibited (Figure 4Cand D)."}
{"Furthermore, endogenousCAMTA1 mRNA as well as protein levels wereelevated, when miR-9 or miR-9* was inhibited (Figure 4Cand D)."}
{"Finally, weanalyzed the effect of miR-16/-424 on VEGFR2, FGFR1, andVEGF expression. HUVECs were transfected with miR-16 ormiR-424 mimics, and the effects on protein and mRNA levelswere analyzed 36 hours posttransfection. As shown in Figure2A to 2C, both miR-16 and miR-424 significantly decreasedVEGFR2, FGFR1, and VEGF protein and mRNA levels."}
{"Finally, weanalyzed the effect of miR-16/-424 on VEGFR2, FGFR1, andVEGF expression. HUVECs were transfected with miR-16 ormiR-424 mimics, and the effects on protein and mRNA levelswere analyzed 36 hours posttransfection. As shown in Figure2A to 2C, both miR-16 and miR-424 significantly decreasedVEGFR2, FGFR1, and VEGF protein and mRNA levels."}
{"Finally, weanalyzed the effect of miR-16/-424 on VEGFR2, FGFR1, andVEGF expression. HUVECs were transfected with miR-16 ormiR-424 mimics, and the effects on protein and mRNA levelswere analyzed 36 hours posttransfection. As shown in Figure2A to 2C, both miR-16 and miR-424 significantly decreasedVEGFR2, FGFR1, and VEGF protein and mRNA levels."}
{"Finally, weanalyzed the effect of miR-16/-424 on VEGFR2, FGFR1, andVEGF expression. HUVECs were transfected with miR-16 ormiR-424 mimics, and the effects on protein and mRNA levelswere analyzed 36 hours posttransfection. As shown in Figure2A to 2C, both miR-16 and miR-424 significantly decreasedVEGFR2, FGFR1, and VEGF protein and mRNA levels."}
{"Finally, weanalyzed the effect of miR-16/-424 on VEGFR2, FGFR1, andVEGF expression. HUVECs were transfected with miR-16 ormiR-424 mimics, and the effects on protein and mRNA levelswere analyzed 36 hours posttransfection. As shown in Figure2A to 2C, both miR-16 and miR-424 significantly decreasedVEGFR2, FGFR1, and VEGF protein and mRNA levels."}
{"Finally, weanalyzed the effect of miR-16/-424 on VEGFR2, FGFR1, andVEGF expression. HUVECs were transfected with miR-16 ormiR-424 mimics, and the effects on protein and mRNA levelswere analyzed 36 hours posttransfection. As shown in Figure2A to 2C, both miR-16 and miR-424 significantly decreasedVEGFR2, FGFR1, and VEGF protein and mRNA levels."}
{"Finally, weanalyzed the effect of miR-16/-424 on VEGFR2, FGFR1, andVEGF expression. HUVECs were transfected with miR-16 ormiR-424 mimics, and the effects on protein and mRNA levelswere analyzed 36 hours posttransfection. As shown in Figure2A to 2C, both miR-16 and miR-424 significantly decreasedVEGFR2, FGFR1, and VEGF protein and mRNA levels."}
{"To assess whether miR-758 regulates the expression ofthese targets, we transfected H4 cells with miR-758. As seenin Figure 6C, miR-758 overexpression reduced significantlythe mRNA expression of SLC38A1, IGF1, NTM, STXBP1,and EPHA7, suggesting an important role of miR-758 inregulating neurological functions."}
{"To assess whether miR-758 regulates the expression ofthese targets, we transfected H4 cells with miR-758. As seenin Figure 6C, miR-758 overexpression reduced significantlythe mRNA expression of SLC38A1, IGF1, NTM, STXBP1,and EPHA7, suggesting an important role of miR-758 inregulating neurological functions."}
{"To assess whether miR-758 regulates the expression ofthese targets, we transfected H4 cells with miR-758. As seenin Figure 6C, miR-758 overexpression reduced significantlythe mRNA expression of SLC38A1, IGF1, NTM, STXBP1,and EPHA7, suggesting an important role of miR-758 inregulating neurological functions."}
{"Importantly, Fzd6 expressionwas also up-regulated in liver from mice treated onlywith antagomir-194 (Fig. 4C),"}
{"Importantly, Fzd6 expressionwas also up-regulated in liver from mice treated onlywith antagomir-194 (Fig. 4C),"}
{"We verified that miR-17 can binddirectly to the 3 UTR of tgfbr2 (position 2388) and creb1 (position6984) mRNAs (Figure 6B-C) using luciferase reporter assays. InCD4  T cells lacking mir-17-92, the expression levels of TGF RIIand CREB1 were significantly elevated at both the mRNA andprotein levels, and these elevations were completely abolishedwhen the mir-17 gene was reintroduced (Figure 6D-E)."}
{"We verified that miR-17 can binddirectly to the 3 UTR of tgfbr2 (position 2388) and creb1 (position6984) mRNAs (Figure 6B-C) using luciferase reporter assays. InCD4  T cells lacking mir-17-92, the expression levels of TGF RIIand CREB1 were significantly elevated at both the mRNA andprotein levels, and these elevations were completely abolishedwhen the mir-17 gene was reintroduced (Figure 6D-E)."}
{"We verified that miR-17 can binddirectly to the 3 UTR of tgfbr2 (position 2388) and creb1 (position6984) mRNAs (Figure 6B-C) using luciferase reporter assays. InCD4  T cells lacking mir-17-92, the expression levels of TGF RIIand CREB1 were significantly elevated at both the mRNA andprotein levels, and these elevations were completely abolishedwhen the mir-17 gene was reintroduced (Figure 6D-E)."}
{"The cells were transiently transfectedwith miR-150 mimic and the expression of MUC4 was examined. Ourdata revealed no apparent change in MUC4 expression at the transcriptlevel (Figure 1C), whereas it was significantly downregulated atthe protein level (Figure 1D) in miR-150 mimic transfected cells ascompared with non-targeting control (miR-NC) mimic transfectedcells. Our data suggest that miR-150 downregulates MUC4 expressionthrough a posttranscriptional mechanism."}
{"Further analysis demonstrated 50% reduction of endogenous TIMP3 mRNA levelin OHTR cells as well as miR-221/222-overexpressing cellswhen compared with MCF-7 cells and when miR-181b wastransiently overexpressed (Fig. 1E). In addition, a markedreduction (75%) in TIMP3 protein was observed in OHTRcells when compared with an  50% reduction when individualmiRs were overexpressed (Fig. 1F)."}
{"Further analysis demonstrated 50% reduction of endogenous TIMP3 mRNA levelin OHTR cells as well as miR-221/222-overexpressing cellswhen compared with MCF-7 cells and when miR-181b wastransiently overexpressed (Fig. 1E). In addition, a markedreduction (75%) in TIMP3 protein was observed in OHTRcells when compared with an  50% reduction when individualmiRs were overexpressed (Fig. 1F)."}
{"Further analysis demonstrated 50% reduction of endogenous TIMP3 mRNA levelin OHTR cells as well as miR-221/222-overexpressing cellswhen compared with MCF-7 cells and when miR-181b wastransiently overexpressed (Fig. 1E). In addition, a markedreduction (75%) in TIMP3 protein was observed in OHTRcells when compared with an  50% reduction when individualmiRs were overexpressed (Fig. 1F)."}
{"Further analysis demonstrated 50% reduction of endogenous TIMP3 mRNA levelin OHTR cells as well as miR-221/222-overexpressing cellswhen compared with MCF-7 cells and when miR-181b wastransiently overexpressed (Fig. 1E). In addition, a markedreduction (75%) in TIMP3 protein was observed in OHTRcells when compared with an  50% reduction when individualmiRs were overexpressed (Fig. 1F)."}
{"To confirm that Lats2 is a target gene of rno-miR-31 in culturedVSMCs, both gain-of-function and loss-of-functionapproaches were applied. As expected, LATS2 was up-regulatedby miR-31 inhibitor (Fig. 6D) and down-regulated by AdmiR-31 (Fig. 6E) at the protein level. It is well known that miRNAscould regulate their target gene expression via inhibitingtranslation and/or promoting degradation of target genes (1, 2).To determine whether rno-miR-31 could cause the degradationof its target Lats2, we detected Lats2 mRNA levels incultured VSMCs transfected with vehicle, Ad-GFP, orAd-miR-31 respectively. Interestingly, overexpression of rnomiR-31 by Ad-miR-31 decreased the Lats2 mRNA level,"}
{"To confirm this possibility wedetermined whether over-expression or inhibition ofmiR-155 would lead to significant changes in SOCS-1mRNA and protein levels."}
{"To assess whether miR-206 directly regulates BDNFexpression, a synthetic miR-206 precursor RNA wastransiently transfected into low confluency proliferatingmyoblasts and harvested for RNA analysis after 18‚Äì24 h.This treatment increased mature miR-206 levels and caused both total and BDNF-L mRNA levels to be reduced by 50% as measured by qRT-PCR (p < 0.01) (Fig. 3a)."}
{"To assess whether miR-206 directly regulates BDNFexpression, a synthetic miR-206 precursor RNA wastransiently transfected into low confluency proliferatingmyoblasts and harvested for RNA analysis after 18‚Äì24 h.This treatment increased mature miR-206 levels and caused both total and BDNF-L mRNA levels to be reduced by 50% as measured by qRT-PCR (p < 0.01) (Fig. 3a)."}
{The PTN mRNA and protein expression were examined by RT-PCR (Fig. 3C) or western blotting (Fig. 3D). MiR-143 significantly suppressed PTN protein level without affecting mRNA expression, }
{"Furthermore, the introduction of let-7a-mimics or let-7a-inhibitor into DLD1 cells caused downregulation and upregulation of NIRF expression, respectively, as demonstrated by qRT-PCR and Western blot analysis (Fig. 2B and C). Taken together, these data indicate that let-7a may regulate NIRF expression through let-7a-binding sites at the 3‚Ä≤-UTR of NIRF."}
{To identify whether Srebf1 could be a true target mRNA of miR-21 we introduced miR-21inhibitor (LNA-21) and control oligonucleotides (LNA-scr) into INS-1E cells, and extracted RNA and protein from these. MessengerRNA levels of Srebf1 increased by about 30% after miR-21 knock-down (Fig. 5E). Also SREBP1 protein levels increased approximately 50% after miR-21 knock-down compared with a LNA-scr (Fig. 5G, H). }
{"Klf4 mRNA levels decreased 20% in miR-137 overexpressing cortical neurons when compared with thenull-vector transfected neurons (figure 6B)."}
{"Transfection of cIELs with anti‚ÄìmiR-223 resulted in an increasein Roquin gene expression and a decrease in IL-17A gene expression;miR-223 suppressed Roquin expression and enhancedIL-17A expression (Fig. 4A), suggesting a role for miR-223 inRoquin regulation. This was confirmed by luciferase reporterassays, which demonstrated that the 39 UTR of the Roquin genewas a target for miR-223, as seen by the negative regulatoryeffects (Fig. 4B)."}
{"As shown inFigure 4A and B, the miR-622 mimic did not affect the levels ofE2f1, c-myc or Cdk6 proteins but exhibited a significant 0.35 ¬±0.08-fold reduction in the level of K-Ras protein in 16HBE-T cellstransfected with the miR-622 mimic,However, the miR-622 mimic did not affectthe K-Ras mRNA expression levels, suggesting that miR-622 regulatesK-Ras mRNA translation without affecting accumulation levels(Figure 4C)."}
{"As shown inFigure 4A and B, the miR-622 mimic did not affect the levels ofE2f1, c-myc or Cdk6 proteins but exhibited a significant 0.35 ¬±0.08-fold reduction in the level of K-Ras protein in 16HBE-T cellstransfected with the miR-622 mimic,However, the miR-622 mimic did not affectthe K-Ras mRNA expression levels, suggesting that miR-622 regulatesK-Ras mRNA translation without affecting accumulation levels(Figure 4C)."}
{"As shown inFigure 4A and B, the miR-622 mimic did not affect the levels ofE2f1, c-myc or Cdk6 proteins but exhibited a significant 0.35 ¬±0.08-fold reduction in the level of K-Ras protein in 16HBE-T cellstransfected with the miR-622 mimic,However, the miR-622 mimic did not affectthe K-Ras mRNA expression levels, suggesting that miR-622 regulatesK-Ras mRNA translation without affecting accumulation levels(Figure 4C)."}
{"However, no significant change of 4E-BP1 mRNA level was found after transfection of miR-125b mimic or inhibitor(Figures 3A and 3B),"}
{"Such miR-145 overexpressiongreatly decreased the levels of SOX9 both at the mRNA andparticularly at the protein level (Fig. 2, B andC)."}
{"In addition, overexpression of selected miR was alsoperformed in the Y1 mouse adrenocortical cell line. Upontransfection of miR-101a, a significant down-regulationof the Nr3c1 expression ratio could be demonstrated bothat the mRNA (control: 1 0.107, vs. 0.688 0.122; P 0.05) (Fig. 5B) and the protein level (control: 1 0.07, vs.0.782   0.01; P   0.05) (Fig. 5C)."}
{"Similarly, transfectionof miR-142-3p resulted in a reduction of the Nr3c1 expressionratio in both the mRNA (control: 1   0.107, vs.0.891   0.017; P   0.05) and the protein level (control:1 0.107, vs. 0.933 0.055; P 0.05),"}
{"Furthermore, we showed that miR-210 can suppressthe messenger RNA (mRNA) and protein levels ofVMP1 in HCC cells (Fig. 4D,E) and that there isdose-dependence between the expression of VMP1 andmiR-210 (Supporting Fig. 3)."}
{In NIH3T3 cells transfected with either PCMV-Prm2 or -TP2 plasmid, mRNA of Prm2 or TP2 was not altered by the overexpression of miR-469 (p>0.05) (Fig. 7A). However, the level of protein expression in either case was significantly decreased (Fig. 7B) by overexpression of miR-469.}
{In NIH3T3 cells transfected with either PCMV-Prm2 or -TP2 plasmid, mRNA of Prm2 or TP2 was not altered by the overexpression of miR-469 (p>0.05) (Fig. 7A). However, the level of protein expression in either case was significantly decreased (Fig. 7B) by overexpression of miR-469.}
{In NIH3T3 cells transfected with either PCMV-Prm2 or -TP2 plasmid, mRNA of Prm2 or TP2 was not altered by the overexpression of miR-469 (p>0.05) (Fig. 7A). However, the level of protein expression in either case was significantly decreased (Fig. 7B) by overexpression of miR-469.}