sort by

35 publications mentioning rno-mir-92a-1

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-92a-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 242
In the current study, the expression of the miR-17-92 cluster was up-regulated in H/R H9c2 cardiomyocytes: the expression of miR-92a was significantly up-regulated by 2.78-fold over the control (P<0.01 vs. [score:11]
Taken together, the current study indicated that inhibition of miR-92a can attenuate cardiomyocyte apoptosis induced by H/R via the up-regulation of SMAD7 and down-regulation of nuclear NF-κB p65. [score:9]
The present study demonstrated that inhibition of miR-92a significantly increased protein levels of SMAD7, but did not affect Smad7 mRNA levels, indicating that miR-92a inhibits the protein translation at the post-transcriptional level, but does not promote Smad7 mRNA degradation. [score:7]
Smad7 is a Target of miR-92aBioinformatic analysis using MiRanda, miRDB, miRwalk and TargetScan suggested Smad7 as a target of miR-92a. [score:7]
Bonauer et al. demonstrated that the expression level of miR-92a was up-regulated 24 h after coronary artery ligation in mice [19]. [score:6]
Zhang et al. demonstrated that both overexpression and down-regulation of miR-92a could have pro-angiogenic effects in human umbilical endothelial cells (HUVEC) [25]. [score:6]
At 50 nM, the miR-92a inhibitor significantly down-regulated miR-92a by 2.43±0.06-fold (P<0.01 vs. [score:6]
qRT-PCR analysis of endogenous Smad7 mRNA levels in the cardiomyocytes transfected with miR-92a inhibitor, or co -transfected with miR-92a inhibitor and siRNA-Smad7. [score:5]
Inhibiting miR-92a can attenuate myocardiocyte apoptosis induced by hypoxia/reoxygenation by targeting Smad7. [score:5]
Bioinformatic analysis using MiRanda, miRDB, miRwalk and TargetScan suggested Smad7 as a target of miR-92a. [score:5]
A. qRT-PCR analysis of endogenous Smad7 mRNA levels in the cardiomyocytes transfected with miR-92a inhibitor, or co -transfected with miR-92a inhibitor and siRNA-Smad7. [score:5]
Cytosolic NF-κB p65 was not affected by transfection with miR-92a inhibitor, or co-transfection with miR-92a inhibitor and siRNA-Smad7 (Figure 7C). [score:5]
The expression levels of miR-92a and Smad7 mRNA were determined using qRT-PCR, normalized to U6, and expressed as the fold change relative to the control (** P<0.01 vs. [score:5]
Inhibition of miR-92a promotes SMAD7 expression and activates the Smad7/NF-κB signaling pathway. [score:5]
D. Western blotting assays for the nuclear NF-κB p65 protein levels in the cardiomyocytes transfected with miR-92a inhibitor, or co -transfected with miR-92a inhibitor and siRNA-Smad7. [score:4]
To examine whether miR-92a regulates the expression of Smad7, we used a dual luciferase psiCheck-2 reporter plasmid (Promega, Madison, WI, USA) to generate a reporter plasmid harboring the Smad7 3′-UTR. [score:4]
A luciferase reporter assay indeed demonstrated that miR-92a could inhibit Smad7 expression. [score:4]
C. Western blotting assays for the cytosolic NF-κB p65 protein levels in the cardiomyocytes transfected with miR-92a inhibitor, or co -transfected with miR-92a inhibitor and siRNA-Smad7. [score:4]
MiR-92a directly regulates Smad7 expression via 3′-UTR site. [score:4]
B. Western blotting assays for the SMAD7 protein level in the cardiomyocytes transfected with miR-92a inhibitor, or co -transfected with miR-92a inhibitor and siRNA-Smad7. [score:4]
The miR-92a inhibitor did not affect the level of Smad7 mRNA (Figure 7A). [score:3]
Western blotting (Figure 7B) revealed increased level of SMAD7 by the miR-92a inhibitor (in comparison to H/R alone, P<0.05). [score:3]
In a preliminary bioinformatic analysis, we identified SMAD family member 7 (Smad7) as a potential target for miR-92a. [score:3]
H9c2 cells were plated in 24-well plates and cultured to 80–90% confluence for transient transfection with the miR-92a inhibitor (50 nM) or NC (50 nM), respectively. [score:3]
Smad7 is a Target of miR-92a. [score:3]
Based on the Hinkel et al. study that demonstrated reduced I/R -induced cell apoptosis and necrosis in HL-1 cells upon miR-92a inhibition in a murine myocyte-like cell line [20], we boldly speculate that our findings may be generalized to other species although such a generalization clearly needs to be verified. [score:3]
Transfection of miR-92a inhibitor significantly decreased the level of miR-92a in cultured H9c2 cells under normoxic conditions, respectively (Figure 2A). [score:3]
Co-transfection with siRNA-Smad7 attenuated the effects of the miR-92a inhibitor. [score:3]
The effects of the miR-92a inhibitor on nuclear NF-κB p65 were attenuated by co-transfection with siRNA-Smad7 (Figure 7D). [score:3]
The complementary nucleotides between miR-92a and the target region of Smad7 3′-UTR are indicated with short vertical lines. [score:3]
A preliminary bioinformatics analysis identified Smad7 as a target for miR-92a. [score:3]
Transfection with miR-92a inhibitor significantly decreased the percentage of necrosis induced by H/R (6.16±0.35%, P<0.05 vs. [score:3]
In the study, we found that transfection with miR-92a inhibitor could attenuate myocardial injury and apoptosis induced by hypoxia/reoxygenation (H/R) in cultured rat H9c2 myocardiocytes cells. [score:3]
The observed effects of the miR-92a inhibitor were also attenuated by co-transfection with siRNA-Smad7. [score:3]
The construct with a mutated targeting fragment (TATACCG) in the 3′-UTR of Smad7 lacking the putative miR-92a binding sequence was used as a mutated control. [score:3]
Based on bioinformatic analyses, Smad7 was identified as a target of miR-92a. [score:3]
Effects of the miR-92a inhibitor were attenuated by co-transfection with siRNA-Smad7. [score:3]
Neither mock nor NC RNA transfection affected miR-92a expression under normoxic cultures. [score:3]
The miR-92a inhibitor dramatically reduced the release of lactate dehydrogenase and malonaldehyde, and attenuated cardiomyocyte apoptosis. [score:3]
The present study showed that the inhibition of miR-92a could significantly reduce H/R -induced myocardiocyte injury and apoptosis. [score:3]
The H/R -induced MDA release was significantly decreased by the miR-92a inhibitor (26.93±1.59 ng/mL, P<0.01 vs. [score:3]
Despite of our findings, whether Smad7 is the most important target of miR-92a in cardiomyocytes (and thus the therapeutic potentials) remains unknown. [score:3]
0100298.g002 Figure 2H9c2 cells were transfected with miR-92a inhibitor or siRNA-Smad7 with Lipofectamine2000 for 2 days. [score:3]
The miR-92a inhibitor significantly decreased LDH release in response to H/R (10.93±1.35 ng/mL, P<0.01 vs. [score:3]
The effects of miR-92a inhibitor were also attenuated by co-transfection with siRNA-Smad7. [score:3]
The protein level of SMAD7 was increased by the miR-92a inhibitor. [score:3]
0100298.g006 Figure 6 H9c2 cells were plated in 24-well plates and cultured to 80–90% confluence for transient transfection with the miR-92a inhibitor (50 nM) or NC (50 nM), respectively. [score:3]
H9c2 cells were transfected with miR-92a inhibitor or siRNA-Smad7 with Lipofectamine2000 for 2 days. [score:3]
Inhibition of miR-92a Protects against H/R -induced Injury and Apoptosis. [score:3]
Increased expression of miR-92a was the most prominent at 2.78-fold. [score:3]
Prior to hypoxia/reoxygenation, cells were transfected by miR-92a inhibitor. [score:3]
The miR-92a inhibitor increased SMAD7 protein level and decreased nuclear NF-κB p65 protein. [score:3]
The effects of miR-92a inhibitor were attenuated by co-transfection with siRNA-Smad7. [score:3]
Hinkel and colleagues demonstrated that inhibiting miR-92a protects against myocardial I/R injury in a porcine mo del [20]. [score:3]
Gene levels in normoxic H9c2 cardiomyocytes transfected with miR-92a inhibitor (A) or siRNA-Smad7 (B). [score:3]
In our previous study [12], we found that miR-17, miR-19a, miR-20a, miR-19b and miR-92a, but not miR-18a, were highly expressed in the heart of C57BL/6 mice. [score:3]
Transfection with miR-92a inhibitor significantly decreased the percentage of apoptosis induced by H/R (18.56±2.08%, P<0.01 vs. [score:3]
For example, Hinkel et al demonstrated that inhibition of miR-92a significantly reduced I/R -induced cell apoptosis and necrosis in HL-1 cells [20]. [score:3]
Nuclear NF-κB p65 was significantly decreased by the miR-92a inhibitor (in comparison with H/R alone, P<0.05). [score:3]
MiR-92a mimic, inhibitor and matched negative control (NC) were synthesized by GenePharma, Shanghai, China. [score:2]
Recent studies reported that knockdown of miR-92a could attenuate ischemia/reperfusion -induced myocardial injury. [score:2]
Accordingly, we also examined the possible involvement of Smad7 in the protective action of miR-92a. [score:1]
Growing evidence also supports a pivotal role for miR-92a in multiple processes, including tumorigenesis and metastasis [10], cell proliferation and apoptosis [11]. [score:1]
293T cells were co -transfected with psiCheck2 containing the Smad7 3′-UTR and the miR-92a mimic using Lipofectamine 2000 (Invitrogen). [score:1]
Specifically, the 3′-UTR of the Smad7 mRNA contains one binding site for miR-92a (Figure 5A). [score:1]
In comparison with the mutated control, the miR-92a mimic reduced the activity of the luciferase reporter fused with the Smad7 3′-UTR by 41% (Figure 5B). [score:1]
The effect of miR-92a on SMAD7 was observed by immunocytofluorescent staining. [score:1]
A. The potential binding site for miR-92a in the 3′-UTR of Smad7 mRNA. [score:1]
Based on the most remarkable change in response to hypoxia/reoxygenation as reflected by qRT-PCR, miR-92a was selected for subsequent experiments. [score:1]
Put together, our findings suggest that apoptosis in myocardial I/R injury, is mediated, at least partly, through the miR-92a/Smad7/NF-κB p65 pathway. [score:1]
In the present study, we examined the potential anti-apoptotic effects of miR-92a in a rat myocardiocyte cell line, and the possible role of Smad7 in such actions. [score:1]
[1 to 20 of 71 sentences]
2
[+] score: 184
normoxia for 48 h. To confirm whether BM-MSC may inhibit miRNA-23a and miRNA-92a expression in a paracrine manner, we analyzed apoptosis and miRNA expression in vitro. [score:7]
Similarly, our study showed that MSC-released VEGF inhibited the expression of miRNA-23a and miRNA-92a, which induced cardiac apoptosis, thereby inhibiting ischemic injury -induced cardiac apoptosis (Figs 6 and 7). [score:7]
The hypoxia-exposed BM-MSC-conditioned media significantly reduced apoptosis in cardiomyocytes and suppressed the hypoxia -induced up-regulation of miRNA-23a and miRNA-92. [score:6]
In particular, a previous study demonstrated that expression of miRNA-92a was up-regulated 24 h after the induction of MI, and that treatment with antagomir-92a after MI improved left ventricular function and reduced cardiac apoptosis at the border areas of the infarction [45]. [score:6]
To confirm whether paracrine factors derived from BM-MSCs inhibit the hypoxia -induced upregulation of miRNA-23a and miRNA-92a, resulting in reduced cardiac apoptosis, paracrine factors were blocked in hypoxia-exposed BM-MSC-conditioned media using neutralizing antibodies. [score:6]
Inhibition of the hypoxia -induced upregulation of miRNA-23a and miRNA-92a reduced cardiac apoptosis (Fig 5C and 5D). [score:6]
Interestingly, our data indicated that expression of both miRNA-23a and miRNA-92a in the saline -treated group is upregulated at 3 days, but does not increase consistently 4 weeks after saline treatment post-MI (Fig 2). [score:6]
These therapeutic effects of MSC therapy could be mediated by MSC-released paracrine factors including VEGF, which inhibited MI -induced upregulation of miRNA-23a and miRNA-92a. [score:6]
In our present study, we observed that miRNA-23a and miRNA-92a induced cardiac apoptosis and that inhibition of the ischemia -induced upregulation of miRNA-23a and miRNA-92a decreased cardiac apoptosis. [score:6]
To identify the function following knock-down of miRNA-23a and miRNA-92a expression, primary cultured cardiomyocytes were cultured in a six-well plate and were incubated with 40 nM miRNA-23a and miRNA-92a inhibitors (GenePharma, Shanghai, China) using INTERFERin transfection agent (PolyPlus-transfection SA, Illkirch, France), according to the manufacturer’s instructions [29]. [score:6]
To confirm whether cardiac miRNA-23a and miRNA-92a induce cardiac apoptosis, we inhibited miRNA-23a and miRNA-92a by miRNA inhibitor transfection. [score:5]
MSC-released VEGF inhibited miRNA-23a and miRNA-92a expression, thereby improving cardiac apoptosis in the rat mo del of MI. [score:5]
Second, We could not establish inhibition of cardiac miRNA-23a and miRNA-92a expression in vivo by MSC-derived VEGF. [score:5]
The results show that VEGF released from transplanted BM-MSCs inhibited the expression of miRNA-23a and miRNA-92a in cardiomyocytes, which led to decrease in apoptosis and fibrosis in the infarcted myocardium. [score:5]
They also identified Smad7 as the target of miRNA-92a; treatment with miRNA-92a inhibitor increased the protein levels of Smad7 although the Smad7 mRNA levels remained unchanged. [score:5]
0179972.g005 Fig 5(A, B) Transfection efficiency of the miRNA-23a inhibitor (A) and miRNA-92a inhibitor (B) was determined by real-time PCR using TaqMan probes. [score:5]
In cultured cardiomyocytes, the transfection of miRNA-23a and miRNA-92a inhibitors significantly abolished the expression level of miRNA-23a and miRNA-92a (Fig 5A and 5B). [score:5]
Quantitative analysis of apoptotic cells in cardiomyocytes transfected either with miRNA-23a inhibitor (C) or miRNA-92a inhibiton (D). [score:5]
BM-MSC-conditioned media inhibits miRNA-23a and miRNA-92a expression and apoptosis in vitro. [score:5]
S5 FigMiRNA-23a (A) and miRNA-92a (B) expression was not regulated by depending on presence or absence of MCP-1 in BM-MSCs hypoxic-conditioned media. [score:4]
VEGF secreted from BM-MSCs regulates hypoxia -induced miRNA-23a and miRNA-92a expression in vitro. [score:4]
First, we were not able to investigate the detailed mechanisms regarding the role of miRNA-23a and miRNA-92a in cardiomyocytes, indicating downregulation of miRNAs by the inhibitory effects of VEGF. [score:4]
Because the expression of miRNA-23a and miRNA-92a was validated to be consistent with the microarray data and showed simultaneously that highest regulated by BM-MSC treatment in the real-time PCR, we focused on miRNA-23a and miRNA-92a. [score:4]
In this study, we showed that VEGF acts upstream of the miRNA-23a and miRNA-92a inhibition pathway in cardiomyocytes, and plays a key role in the therapeutic effects of MSC transplantation in a rat mo del of MI (Fig 6). [score:3]
The effects of VEGF secreted from BM-MSCs on hypoxia -induced miRNA-23a (A) and miRNA-92a (B) expression. [score:3]
Moreover, the regional abolishment of miRNA-92a was shown to improve myocardial ischemia/reperfusion injury in a large animal mo del, suggesting that HL-1 cardiomyocytes treated with miRNA-92a inhibitor are resistant to hypoxia/reoxygenation -induced cell death [16]. [score:3]
MiRNA-23a (A) and miRNA-92a (B) expression in response to treatment with BM-MSCs in comparison with saline or sham at 3 days or 4 weeks after treatment. [score:3]
The expression levels of miRNA-23a and miRNA-92a were significantly higher in hypoxia-exposed cardiomyocytes treated with VEGF-neutralizing antibody than in those not treated with VEGF-neutralizing antibody. [score:3]
In a recent study, Zhang et al. reported that inhibition of miRNA-92a was able to significantly alleviate apoptosis caused by hypoxia/reoxygenation in H9c2 cardiomyocytes [46]. [score:3]
Inhibition of miRNA-23a and miRNA-92a prevents apoptosis of cardiomyocytes. [score:3]
0179972.g006 Fig 6The effects of VEGF secreted from BM-MSCs on hypoxia -induced miRNA-23a (A) and miRNA-92a (B) expression. [score:3]
0179972.g007 Fig 7 Transplanted BM-MSCs release VEGF, which inhibits the MI -induced miRNA-23a and miRNA-92a, thereby blocking cardiomyocytes apoptosis. [score:3]
The neutralization of VEGF in hypoxia-exposed BM-MSC-conditioned media showed a significantly reversed influence on the reduced expression of miRNA-23a and miRNA-92a by hypoxia-exposed BM-MSC-conditioned media (Fig 6A and 6B). [score:3]
Indeed, expression of miRNA-23a and miRNA-92a was significantly lower in the BM-MSC -treated group than in the saline -treated group 3 days after treatment, although no significant difference was observed between the BM-MSC -treated group and saline -treated group 4 weeks after treatment (Fig 2A and 2B). [score:3]
Further studies on the targets of miRNA-23a and miRNA-92a are required to determine the underlying mechanisms involved apoptotic cardiomyocytes in MI. [score:3]
MCP-1 released from BM-MSCs has no effect on miRNA-23a and miRNA-92a expression and apoptosis in vitro. [score:3]
Transplanted BM-MSCs release VEGF, which inhibits the MI -induced miRNA-23a and miRNA-92a, thereby blocking cardiomyocytes apoptosis. [score:3]
This is the first study to show that the therapeutic effects of MSCs in a rat mo del of MI are mediated by a reduction in the expression of pro-apoptotic miRNAs such as miRNA-23a and miRNA-92a by MSC-released VEGF. [score:3]
The neutralization of VEGF in hypoxia-exposed BM-MSC-conditioned media significantly reversed the anti-apoptotic effects of hypoxia-exposed BM-MSC-conditioned media on cardiomyocytes (Fig 6C), whereas neutralizing MCP-1 had no effect on miRNA-23a and miRNA-92a expression and apoptosis of cardiomyocytes (S5 Fig). [score:3]
To clarify this, further studies involving the treatment of an MSC-transplanted rat mo del with anti-VEGF neutralizing antibodies should be performed to confirm the restoration of miRNA-23a and miRNA-92a expression and subsequent apoptosis of cardiomyocytes after VEGF neutralization. [score:3]
MiRNA-23a (C) and miRNA-92a (D) expression in response to treatment with hypoxia-exposed BM-MSC-conditioned media in comparison without hypoxia-exposed BM-MSC-conditioned media in hypoxia. [score:3]
In recent studies, miRNAs, including miRNA-15b [14], miRNA-34a [15], miRNA-92a [16], and miRNA-320 [17] have been reported to be involved in the regulation of cardiomyocyte apoptosis after MI. [score:2]
In a real-time PCR assay using TaqMan probes, the expression levels of miRNA-23a and miRNA-92a were significantly higher in the 48 h hypoxia-exposed cardiomyocytes than in the normoxia-exposed cardiomyocytes and were also significantly lower in the hypoxia-exposed cardiomyocytes treated with hypoxia-exposed BM-MSC-conditioned media than in cardiomyocytes not treated with hypoxia-exposed BM-MSC-conditioned media (Fig 4C and 4D). [score:2]
Through a screening microarray experiment, we selected promising candidate miRNAs, miRNA-23a and miRNA-92a, which could explain the mechanisms of the effects of BM-MSC therapy. [score:1]
Cardiac miRNA-23a and miRNA-92a induce cardiac apoptosis. [score:1]
Further studies are required to understand the mechanisms involved in the effects of miRNA-23a and miRNA-92a, specifically regarding the occurrence of apoptosis in cardiomyocytes. [score:1]
[1 to 20 of 46 sentences]
3
[+] score: 39
The mRNA encoding the cyclin dependent kinase inhibitor 1c (Cdkn1c) was up-regulated 3-fold in E13 ENPs and is predicted to be targeted by three miRNAs that were down-regulated: miR-92, miR-222, and miR-363-3p. [score:11]
Notably, we found miR-222, miR-291-3p, miR-183, miR-363-3p, miR-92, miR-19a and miR-145 as down-regulated miRNAs between E11 and E13 and whose expression was negatively correlated with the expression of their predicted targets. [score:10]
Focusing on the down-regulated miRNAs that had a significant negative correlation in Figure 6, we performed network analysis and identified miR-92, miR-183, miR-222 and miR-291-3p as predicted to target multiple TFs that were up-regulated in E13 ENPs (Figure 8). [score:9]
Additional support for this hypothesis was provided by the miRNA-TF mRNA network analysis in Figure 8. We found four down-regulated miRNAs (miR-92, miR-183, miR-222 and miR-291-3p) that were predicted to target multiple TFs, which were up-regulated in E13 ENPs. [score:9]
[1 to 20 of 4 sentences]
4
[+] score: 30
Activities of luciferases with putative target 3′-UTR sequences were generally decreased by their corresponding miRNAs (Fig. 4b), although Kcna1 and Dpp10 3′-UTRs were not targeted by miR-92a or miR-18a, respectively. [score:5]
Significant mechanical allodynia was observed in rats overexpressing miR-18a, miR-19a, miR-19b or miR-92a, but not in those overexpressing miR-17 or miR-20a (Fig. 2e). [score:5]
The number of putative target genes for miR-18a, miR-19a/b (miR-19a and miR-19b have the same seed sequence) and miR-92a were 695, 1,448 and 1,138, respectively (a total of 2,834 genes). [score:3]
Only the cluster members whose overexpression reduced the mechanical paw withdrawal threshold (miR-18a, miR-19a, miR-19b and miR-92a) were examined. [score:3]
Interestingly, miR-92a antisense RNA also significantly suppressed thermal hyperalgesia, to a lesser extent (Supplementary Fig. 6a). [score:3]
AAV vectors expressing either a control AAV vector or mixture of AAV vectors encoding TuD antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a were administered 7 days after SNL. [score:3]
L5 DRGs were obtained 28 days after SNL from rats injected with mixture of AAV vectors expressing antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a 7 days after SNL. [score:3]
Furthermore, the established mechanical allodynia was reversed by injection of a mixture of AAV vectors encoding antisense RNAs against miR-18a, miR-19a, miR-19b and miR-92a 7 days after SNL (Fig. 3b). [score:1]
Error bars are s. e. m. * P<0.05, ** P<0.01 and *** P<0.001 (K [V]1.1, P=0.014 for miR-17-92 and P=0.034 for miR-18a; K [V]1.4, P<0.001 for miR-17-92; K [V]3.4, P<0.001 for miR-17-92, P=0.047 for miR-19b and P=0.009 for miR-92a; K [V]4.3, P=0.031 for miR-17-92; K [V]7.5, P=0.002 for miR-17-92, P=0.048 for miR-19a and P=0.013 for miR-19b; DPP10, P=0.003 for miR-17-92 and P=0.043 for miR-92a; Na [V]β1, P=0.002 for miR-17-92 and P=0.030 for miR-19b), Dunnett’s test. [score:1]
As miR-19a/b and miR-92a have two predicted binding sites for Kcna4 3′-UTR and Kcnc4 3′-UTRs, respectively, both sites were mutated. [score:1]
In this context, therapeutic manipulation of miR-17-92 cluster would be advantageous, as its components miR-18a, miR-19a/b and miR-92a collectively modulate multiple potassium channel α subunits and auxiliary subunits in DRG neurons. [score:1]
Clone IDs of TuD were as follows: NC000001 (negative control), RH000611 (miR-17), RH000323 (miR-18a), RH000643 (miR-19a), RH000352 (miR-19b), RH000277 (miR-20a) and RH000184 (miR-92a). [score:1]
[1 to 20 of 12 sentences]
5
[+] score: 15
In details, miR-101a was down-regulated, and it decreased cell number in the G2-M phase with consistently increases in cell number in the G1 or S phases; meanwhile, miR-92a, miR-25, miR-93, and miR-106b were up-regulated, and they decreased the G1 cell population while concomitantly increasing the accumulation of cells in the S and G2 phases. [score:7]
As we expected, miR-106b, miR-93, miR-25 and miR-92a were significantly up-regulated at 24 and 36 hours after 2/3 PH, and miR-101a was down-regulated at 12, 24 and 36 hours after 2/3 PH (Supplementary Figure 5). [score:7]
As demonstrated above, miR-92a, miR-25, miR-93, and miR-106b are associated with faster entry into the S and/or G2 phases. [score:1]
[1 to 20 of 3 sentences]
6
[+] score: 12
Of these, miR-500-3p, miR-23b-3p, miR-200a-3p, miR-19b-3p, miR-92a-1-5p, miR-21-5p, miR-21-3p, miR-1843-3p, miR-223-3p, miR-3473, and miR-129-2-3p were found to be upregulated, whereas miR-92b-3p, miR-3102, and miR-3577 were found to be downregulated in the rat brain. [score:7]
Some of the differentially expressed miRNAs were previously reported (miR-223, miR-129, and miR-92) [4, 5], which support our results. [score:3]
miR-92 was previously reported as regulator of angiogenesis and cardiac ischemic/reperfusion injury [25, 39]. [score:2]
[1 to 20 of 3 sentences]
7
[+] score: 10
Since co-expressed miRNAs have been shown to coordinately regulate canonical cell signaling networks associated with cell death and cell survival [18], it is notable that we found that all members of the miR-17-92 cluster (miR-17-5p, miR-18a, miR-19a, miR-92a) are upregulated after TBI and these miRNAs co-target and possibly negatively co-regulate many TBI-altered genes. [score:10]
[1 to 20 of 1 sentences]
8
[+] score: 10
IPA identified 4 focus miRNAs related to metastasis and upper gastrointestinal tract cancer (≥4 fold change) that were downregulated in metastasis positive samples versus metastasis negative samples: 1) miR-92a-3p (p = 0.0001, fold change >14), miR-141-3p (p = 0.0022, fold change >9), miR-451-1a (p = 0.0181, fold change >12) and miR133a-3p (p = 0.0304, fold change >9) (S2 Fig. ). [score:4]
miRNome analysis identified four down-regulated miRNAs in metastasis positive primary tumors compared to metastasis negative tumors: miR-92a-3p (p=0.0001), miR-141-3p (p=0.0022), miR-451-1a (p=0.0181) and miR133a-3p (p=0.0304). [score:3]
The 4 miRNAs (miR-92a-3p, miR-451a, miR-141-3p, and miR-133-3p) were significantly down regulated in metastasis positive tumors. [score:2]
The 4 focus miRNAs symbols miR-92a-3p, miR-141-3p, miR-451-1a, and miR133a-3p were mapped from the dataset ID rno-miR-32-5p, rno-miR-141-3p, rno-miR-451-5p, and rno-miR-133b-3p respectively. [score:1]
[1 to 20 of 4 sentences]
9
[+] score: 7
Additionally, Yuan et al. determined that thousands of miRNAs, such as miR-21, miR-17, and miR-92a, are up-regulated, whereas others, such as miR-205 and miR-145, are downregulated in the setting of femoral head repair using high-throughput gene chip technology [22]. [score:7]
[1 to 20 of 1 sentences]
10
[+] score: 7
MiR-92, another member of the cluster, has been shown to regulate myocardial angiogenesis through targets distinct from those of miR20a, including integrin subunit alpha5 [14]. [score:4]
Note relatively higher expression of 3′ members of the cluster, miR-20a, miR-19b, and miR-92. [score:3]
[1 to 20 of 2 sentences]
11
[+] score: 7
Although the evidence suggests that cell type-specific responses are possible in response to miR-17-92, downregulation of miR-92a specifically triggers macrophage infiltration of the tumor stroma, promotes cell migration and decreases survival in breast cancer patients [48]. [score:4]
Other miRs which were more abundant in CDC-EVs vs MSC-EVs included miR-124, miR-210, miR-92 and miR-320. [score:1]
Another miR similarly abundant in human- and rat-CDC-EVs, and significantly higher compared with MSC-EVs, was miR-92, a member of the miR-17-92 cluster, and an important regulator of cancer and aging [46]. [score:1]
Next, in comparing EV miRs (Figure 6B), we observed that miR-146a was exclusive for human CDC-EVs and miR-92a was exclusive for human and rat CDC-EVs among the most abundant miRs. [score:1]
[1 to 20 of 4 sentences]
12
[+] score: 7
Only five miRNAs (mmu-miR-451, mmu-miR-223, mmu-miR-92a, mmu-miR-200c, and mmu-miR-873) were differentially expressed, implying that the majority of miRNA downregulation associated with obesity could be reversed by LFD treatment. [score:6]
Some of the circulating miRNAs identified in this study have also been reported in the adipose tissue of DIO mice or implicated in adipogenic processes [11– 13], including Let-7, miR-103, miR-15, the miR-17-92 cluster (miR-17, miR-20a, and miR-92a), miR-21, miR-221, and miR-30b. [score:1]
[1 to 20 of 2 sentences]
13
[+] score: 6
miR-17 is a member of the miR-17/92 cluster, one of so far, the best-studied microRNA clusters that codes six mature miRNAs: miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1. Members of this cluster are expressed in a variety of tissues and carry out essential functions both in normal development and in diseases. [score:6]
[1 to 20 of 1 sentences]
14
[+] score: 6
Four of these miRNAs exhibited female-biased expression, and two exhibited male biased expression (miR-92a and miR-221). [score:5]
Among the 65 sex-biased DEMs, only 6 (miR-92a, miR-221, miR-374, miR-505*, miR-532-3p, and miR-652) are encoded on the X-chromosome. [score:1]
[1 to 20 of 2 sentences]
15
[+] score: 6
While the reduction in expression of miR-17-5p, miR-18a, miR-20a, and miR-92 were well coordinated in transdifferentiation, the expression of miR-19a was not concordant with its neighboring microRNA genes. [score:5]
The genes encoding for miR-17-1/miR-17-5p, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1 are clustered on chromosome 15 [35]. [score:1]
[1 to 20 of 2 sentences]
16
[+] score: 6
Besides, miR-140, miR-181a-5p and miR-451 expression were all highly increased during fracture healing process [18] and miR-21 overexpression [19] or miR-92a knockdown [20] would enhance fracture healing property. [score:6]
[1 to 20 of 1 sentences]
17
[+] score: 5
MiR-363 is a member of the miR-92a family and its 2-week expression is consistent with its role in the formation of vascular endothelial cells during mammalian organ development [42]. [score:4]
IPA infrequently associated a rat miRNA with a miRNA family gene name represented by a human miRNA of different name (e. g., rno-miR-363 is affiliated with miR-92a in gene list mapping); thus, miR-363 is associated with miR-92a in the Ingenuity knowledgebase for purposes of functional analysis. [score:1]
[1 to 20 of 2 sentences]
18
[+] score: 5
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
First, a subgroup of miRNAs (miR-15b-5p, miR-17-5p, miR-18a-5p, miR-19a-3p, miR19b-3p, miR-20a-5p, miR-20b-5p, miR-21-5p, miR-23b-5p, miR-24-3p, miR-27a-3p, miR-92a-3p, miR-93-5p, miR-142-3p, miR-344b-2-3p, miR-431, miR-466b-5p and miR-674-3p) displayed increased expression levels during latency (4 and 8 days after SE), decreased their expression levels at the time of the first spontaneous seizure and returned to control levels in the chronic phase (Fig. 2, Supplementary Fig. S1). [score:5]
[1 to 20 of 1 sentences]
19
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Similarly, within the differentially expressed pool of miRNAs, 10 were identified that are intimately involved in regulating intracellular trafficking pathways, including: miR-7b-5p, miR-9-5p, miR-31-5p, miR-92a-3p, miR-106-5p, miR-126-3p, miR-150-5p, miR-204-5p, miR-222-3p, and miR-322-5p (S2 Fig). [score:4]
[1 to 20 of 1 sentences]
20
[+] score: 4
For example, evidence indicate that let-7, miR-140 and miR-92a are crucial for skeletal development [4– 5]; and deficiency of these miRNAs suppress the proliferation as well as the differentiation of growth plate chondrocytes, leading to a dramatic growth defect [4– 5]. [score:4]
[1 to 20 of 1 sentences]
21
[+] score: 4
Additionally, we examined the effects of other four downregulated miRNAs (miR-23b, miR-92a, miR-27a, and miR-30a; results from microarray). [score:4]
[1 to 20 of 1 sentences]
22
[+] score: 3
Other miRNAs from this paper: rno-mir-21, rno-mir-92a-2
Particularly, changes in the expression profile of miR-21 and miR-92a by high shear stress are associated with an atherogenic protective function [61]. [score:3]
[1 to 20 of 1 sentences]
23
[+] score: 3
Other miRNAs from this paper: rno-mir-92a-2, rno-mir-208a, rno-mir-320, rno-mir-494, rno-mir-208b
For example, miR-92a inhibition using regional locked nucleic acid-92a (LNA-92a) reduces infarct size and post-ischemic loss of function [9]. [score:3]
[1 to 20 of 1 sentences]
24
[+] score: 3
miR-17, miR-92a and miR-127 have been shown to regulate lung development [11, 12]. [score:3]
[1 to 20 of 1 sentences]
25
[+] score: 3
Inhibition of miR-92a reduces infarct size and preserves cardiac function after ischemia reperfusion injury in pigs [1]. [score:3]
[1 to 20 of 1 sentences]
26
[+] score: 3
Murata et al. demonstrated that inhibition of miR-92a enhances fracture healing in mice [12]. [score:3]
[1 to 20 of 1 sentences]
27
[+] score: 3
Other miRNAs from this paper: mmu-mir-30a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-132, mmu-mir-134, mmu-mir-135a-1, mmu-mir-138-2, mmu-mir-142a, mmu-mir-150, mmu-mir-154, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-194-1, mmu-mir-200b, mmu-mir-122, mmu-mir-296, mmu-mir-21a, mmu-mir-27a, mmu-mir-92a-2, mmu-mir-96, rno-mir-322-1, mmu-mir-322, rno-mir-330, mmu-mir-330, rno-mir-339, mmu-mir-339, rno-mir-342, mmu-mir-342, rno-mir-135b, mmu-mir-135b, mmu-mir-19a, mmu-mir-100, mmu-mir-139, mmu-mir-212, mmu-mir-181a-1, mmu-mir-214, mmu-mir-224, mmu-mir-135a-2, mmu-mir-92a-1, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-125b-1, mmu-mir-194-2, mmu-mir-377, mmu-mir-383, mmu-mir-181b-2, rno-mir-19a, rno-mir-21, rno-mir-24-1, rno-mir-27a, rno-mir-30a, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-132, rno-mir-134, rno-mir-135a, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-150, rno-mir-154, rno-mir-181b-1, rno-mir-181b-2, rno-mir-183, rno-mir-194-1, rno-mir-194-2, rno-mir-200b, rno-mir-212, rno-mir-181a-1, rno-mir-214, rno-mir-296, mmu-mir-376b, mmu-mir-370, mmu-mir-433, rno-mir-433, mmu-mir-466a, rno-mir-383, rno-mir-224, mmu-mir-483, rno-mir-483, rno-mir-370, rno-mir-377, mmu-mir-542, rno-mir-542-1, mmu-mir-494, mmu-mir-20b, mmu-mir-503, rno-mir-494, rno-mir-376b, rno-mir-20b, rno-mir-503-1, mmu-mir-1224, mmu-mir-551b, mmu-mir-672, mmu-mir-455, mmu-mir-490, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-504, mmu-mir-466d, mmu-mir-872, mmu-mir-877, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-872, rno-mir-877, rno-mir-182, rno-mir-455, rno-mir-672, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, rno-mir-551b, rno-mir-490, rno-mir-1224, rno-mir-504, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, rno-mir-466d, mmu-mir-466q, mmu-mir-21b, mmu-mir-21c, mmu-mir-142b, mmu-mir-466c-3, rno-mir-322-2, rno-mir-503-2, rno-mir-466b-3, rno-mir-466b-4, rno-mir-542-2, rno-mir-542-3
A comparison of effects of ACTH and DEX shows that both hormones increased the expression miRNA-181b, miRNA-672, and miRNA-100, and significantly decreased the levels of miRNA-92a, and miRNA-466b. [score:3]
[1 to 20 of 1 sentences]
28
[+] score: 3
Among miRNAs that were present at higher levels in colostrum whey, let-7i, miR-148b-3p, miR-27b, and miR-125b-3p affect the function of antigen-presenting cells, and miR-15b, miR-24, miR-92a, miR-181a, miR-181c, and miR-181d affect T cell development and function [29], [30], [35]. [score:2]
On the other hand, other miRNAs such as, let-7i, miR-143, miR-148b-3p, miR-15b, miR-17-5p, miR-24, miR-27b, miR-92a, miR-106b, miR-125b-5p, miR-181a, miR-181c, miR-181d, miR-200c, miR-375, miR-107, miR-141, and miR-370, were present at higher levels in colostrum whey than in mature milk whey (Fig. 6). [score:1]
[1 to 20 of 2 sentences]
29
[+] score: 2
Similarly, miR-92a levels were found increased in acute myeloid and lymphoblastic leukemia cells, and decreased in circulation [28], suggesting complex regulatory processes occurring via the circulatory system. [score:2]
[1 to 20 of 1 sentences]
30
[+] score: 2
The expression patterns of some miRNAs observed in our study are consistent with what were observed in previous studies by using the blot-array and Northern blot assays, i. e. miR-125b, miR-9, and miR-181a [6], as well as miR-29a, miR-138 and miR-92 [53]. [score:2]
[1 to 20 of 1 sentences]
31
[+] score: 2
Moreover, miR-92a, one component of the miR-17-92 cluster important for the function of the immune system, could be regulated by lincRNA 841 (ENSSSCT00000035481, Table S8). [score:2]
[1 to 20 of 1 sentences]
32
[+] score: 1
Among the spleen-specific miRNAs identified, five of them belong to the mir17 miRNA cluster, which comprise miR-17, miR-18, miR-19a, miR-19b, miR-20, miR-25, miR-92, miR-93, miR-106a, and miR-106b [59]. [score:1]
[1 to 20 of 1 sentences]
33
[+] score: 1
On the other hand, a few miRs have been found to promote apoptosis of myocardiocytes, such as miR-26 [29], miR-34 [30], and miR-92 [31]. [score:1]
[1 to 20 of 1 sentences]
34
[+] score: 1
Other miRNAs from this paper: cel-let-7, cel-lin-4, hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-29b-1, mmu-mir-101a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-132, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-199a-1, hsa-mir-199a-1, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-132, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-138-1, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-92a-2, rno-let-7d, rno-mir-7a-1, rno-mir-101b, mmu-mir-101b, hsa-mir-181b-2, mmu-mir-17, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-101-2, cel-lsy-6, mmu-mir-181b-2, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7a-2, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-92a-2, rno-mir-101a, rno-mir-128-1, rno-mir-128-2, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-199a, rno-mir-181a-1, rno-mir-421, hsa-mir-181d, hsa-mir-92b, hsa-mir-421, mmu-mir-181d, mmu-mir-421, mmu-mir-92b, rno-mir-17-2, rno-mir-181d, rno-mir-92b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, mmu-mir-101c, mmu-let-7j, mmu-let-7k, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The probes used were: EAM119 (miR-29b), EAM125 (miR-138), EAM224 (miR-17-5p), EAM234 (miR-199a), EAM131 (miR-92), EAM109 (miR-7), EAM150 (miR-9) and EAM103 (miR-124a). [score:1]
[1 to 20 of 1 sentences]
35
[+] score: 1
MiR-17-5p belongs to the miR-17~92 cluster, located on the human chromosome 13q31, and is a prototypical example of a polycistronic miRNA gene encoding six miRNAs (miR-17-5p, miR-18, miR-19a, miR-19b, miR-20 and miR-92). [score:1]
[1 to 20 of 1 sentences]