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44 publications mentioning rno-mir-125a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-125a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 236
Enrichment analysis suggested that differentially expressed genes in GK compared to BN included more predicted miR-125a target genes than would be expected by chance in adipose tissue (FDR = 0.006 for up-regulated genes; FDR = 0.036 for down-regulated genes) but not in liver (FDR = 0.074 for up-regulated genes; FDR = 0.248 for down-regulated genes). [score:16]
In particular, the enrichment of predicted miR-125a target genes among differentially expressed genes has identified likely target genes and indicates that integrating global miRNA and mRNA expression data may give further insights into miRNA -mediated regulation of gene expression. [score:12]
Since miRNAs can cause degradation of target mRNAs, over -expression of miR-125a in both tissues in the GK rat may down-regulate its target genes in GK relative to BN. [score:10]
We integrated our miRNA results with gene expression data from the same animals and found an enrichment of miR-125a target genes predicted by the miRanda algorithm [32] among genes down-regulated in GK rats in adipose tissue. [score:8]
Though the enrichment of miR-125a target genes predicted by miRanda is an interesting finding, it raises a number of questions, including why both down and up-regulated genes should show significant enrichment of miR-125a target genes, and why stronger enrichment was observed for the tissue with lower fold induction of miR-125a. [score:8]
Specifically, overexpression of miR-125a in these tissues in the GK rat would be expected to down-regulate miR-125a target genes [1, 6, 39]. [score:8]
Although in-silico functional profiling of gene expression data and miR-125a target genes lends some support to the idea that miR-125a over -expression is linked to the hyperglycaemic phenotype, further evidence from other mo del systems or functional studies is certainly desirable. [score:7]
Based on a p-value for differential expression between GK and BN, the most significant change in expression was observed for miR-125a in liver (FC = 5.61, P = 0.001, P [adjusted ]= 0.10); this overexpression was validated using quantitative RT-PCR (FC = 13.15, P = 0.0005). [score:7]
Of particular interest, a proposed functional candidate gene for T2D, Ptges2, is a predicted miR-125a target gene and was significantly down-regulated in both tissues. [score:6]
fat) Click here for file Functional profiling and gene-symbols of differentially expressed genes in GK compared to BN rats in adipose tissue (n = 1075) and liver (n = 233) using GENECODIS Click here for file In-Silico functional profiling of miR-125a targets predicted by miRanda (worksheet 1), TargetScan (worksheet 2), and PicTar (worksheet 3). [score:6]
Two other miR-125a target genes of interest in the context of T2D and obesity are Ppap2c and Sult1a1, both of which were significantly down-regulated in adipose tissue from the GK rat. [score:6]
fat) Functional profiling and gene-symbols of differentially expressed genes in GK compared to BN rats in adipose tissue (n = 1075) and liver (n = 233) using GENECODIS In-Silico functional profiling of miR-125a targets predicted by miRanda (worksheet 1), TargetScan (worksheet 2), and PicTar (worksheet 3). [score:6]
In-silico functional profiling of predicted miR-125a targets and differentially expressed genes indicated that lipid metabolism pathways and MAPK signaling may be dysregulated in the hyperglycaemic state. [score:6]
Three miR-125a target genes (Slc35c2, Umps and Ptges2) were significantly down-regulated in GK rats in both tissues. [score:6]
Specifically, we selected 10,000 random sets of genes that were not predicted targets of miR-125a, with each set containing the same number of genes as predicted targets. [score:5]
We have shown that miR-125a expression is increased in two insulin target tissues in a rat mo del of T2D. [score:5]
This was because the overlap between differentially expressed genes and miR-125a targets occurred largely for genes uniquely predicted by miRanda. [score:5]
Gene expression analysis in the same animals revealed a distinct profile characterizing the hyperglycaemic GK rat, including altered expression of several predicted miR-125 target genes. [score:5]
Furthermore, the current data do not demonstrate whether the expression of any of the genes is dysregulated as a direct consequence of the increased miR-125a levels. [score:5]
In-silico functional analysisBiological pathways defined by KEGG [34] that are enriched among the predicted target genes of miR-125a and the lists of differentially expressed mRNAs found in liver and adipose tissue were identified using the GENECODIS software [35]. [score:5]
Since miR-125a was the top-ranking miRNA in liver, and fifth-ranked in adipose tissue, we hypothesized that target genes of miR-125a would be differentially expressed between GK and BN rats in both tissues. [score:5]
Enrichment of miR-125a target genes among differentially expressed genes. [score:5]
Using the mRNA expression data, we investigated whether predicted miR-125a target genes were differentially expressed in liver or adipose tissue. [score:5]
Biological pathways defined by KEGG [34] that are enriched among the predicted target genes of miR-125a and the lists of differentially expressed mRNAs found in liver and adipose tissue were identified using the GENECODIS software [35]. [score:5]
MiR-125a is over-expressed in liver in hyperglycaemic GK rats relative to normoglycaemic BN rats, and our array data also suggest miR-125a is over-expressed in adipose tissue. [score:5]
In the miRNA data, the most striking finding was the over -expression of miR-125a in both liver and adipose tissue (with nearly 6-fold and 2-fold higher expression, respectively) in GK compared to BN rats. [score:4]
Both miR-125a and miR-125b have been reported to be down-regulated in ovarian [43] and breast cancers [44], with potential roles in cell proliferation and differentiation. [score:4]
One approach to identify genes likely to be regulated by miR-125a is to find those that show a strong negative correlation between their expression and miR-125a levels. [score:4]
MiR-125a and its close homolog miR-125b differ by a single nucleotide [40], and thus share many predicted target genes. [score:3]
BN in liver (FC = 5.62, P = 0.001, P [adjusted ]= 0.10)), and we confirmed this over -expression of miR-125a by RT-PCR (FC = 13.15, two-sided t-test P = 0.0005) (Figure 1). [score:3]
Further functional experiments will help elucidate the role of MAPK signalling in T2D and to what extent increased miR-125a expression may affect this pathway. [score:3]
For both up- and down-regulated genes, there was more overlap in adipose tissue compared to liver, even though miR-125a showed a higher fold induction in liver. [score:3]
The only miRNA that showed some evidence of change in expression in both liver and adipose tissue is miR-125a, which ranked top in the liver and fifth in the GK vs. [score:3]
Experimentally validated target genes of both miR-125a and miR-125b in humans include ERBB2 and ERBB3 [41] and LIN28 [42]. [score:3]
Overlap of target-gene lists predicted for miRNA rno-miR-125a using three algorithms. [score:3]
Predicted targets for miR-125a and in-silico functional profiling. [score:3]
The target gene lists were analysed using the GENECODIS tool to investigate the biological pathways (KEGG) that may be affected by overexpression of miR-125a in liver and, to a lesser extent, adipose tissue. [score:3]
In-silico tools assessing the biological role of predicted miR-125a target genes suggest an over-representation of genes involved in the MAPK signaling pathway. [score:3]
The proportion of random gene sets showing equal or greater overlap as the set of miR-125a target genes was used to estimate the false discovery rate. [score:3]
Further studies at the protein level and translation across species, especially to humans, will be important to elucidate the potential role of miR-125a in T2D pathophysiology. [score:3]
As described above, 3 different algorithms were used to generate target gene lists for miR-125a. [score:3]
Click here for file Overlap of target-gene lists predicted for miRNA rno-miR-125a using three algorithms. [score:3]
When the set of 152 miR-125a target genes was tested, mitogen-activated protein kinase (MAPK) signaling was the only pathway to show significant over-representation (P [adjusted ]= 3 × 10 [-5]). [score:3]
GK and BN rats are also genetically different strains, and it is therefore possible that strain differences unrelated to hyperglycaemia could contribute to the altered expression of miR-125a. [score:3]
MiR-125a also showed over -expression in the GK vs. [score:2]
Figure 1 Relative expression of miR-125a in liver from diabetic GK rats compared to BN rats. [score:2]
Our results suggest that increased miR-125a expression may be a characteristic feature of hyperglycaemic GK rats. [score:1]
In each case, the significance of the overlap (estimated false discovery rate) is calculated as the proportion of 10,000 random sets of non-miR-125 target genes of the same size showing equal or greater overlap. [score:1]
This analysis suggested that increased miR-125a levels may particularly affect genes involved in the MAPK signalling pathway. [score:1]
To further investigate the potential role of miR-125a in T2D, we assessed the functional roles of predicted miR-125a target genes. [score:1]
* miR-125a is shown in this table to illustrate the potential overlap of signals detected in liver and adipose tissue. [score:1]
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2
[+] score: 160
As shown in Fig.   2B, Ucn-1 upregulated significantly the expression of miR-125a-3p and miR-324-3p, meanwhile it downregulated the expression of miR-139-3p. [score:11]
Figure  2 confirms that the addition of Ucn-1 in reperfusion significantly upregulated the expression of miR-125-3p and miR-324-3p, meanwhile it downregulated miR-139-3p. [score:9]
Second, Fig.   6A shows that the transfection of NRVMs with lentivirus over -expressing miR-125a-3p (LV-miR-125a-3p) significantly downregulated the expression of BRCA1, CPT2, MAP3K12, MTFR1, TAZ, and XBP1. [score:8]
We determined that miR-125a-3p inhibited the expression of BRCA1, a well-known tumor suppressor with multiple interacting partners and diverse biological functions [32]. [score:7]
Ucn-1 affords acute cardioprotective effects, but also modulates the expression of miR-125a-3p, miR-324-3p, and miR-139-3p, whose overexpression alters the expression of different genes. [score:7]
Remarkably, the upregulation of miR-125a-3p and miR-324 expression by Ucn-1 involved ERK1/2 activation; whereas, Epac2 was implicated in miR-139-3p and miR-324 regulation. [score:7]
Ucn-1 enhanced significantly the expression of both miR-125a-3p (Fig.   4A) and miR-324-3p (Fig.   4B), meanwhile Ucn-1 downregulated miR-139-3p (Fig.   4C), confirming the data obtained in perfused hearts (Fig.   2B). [score:6]
We observed that Ucn-1 differentially regulates the expression of miR-125a-3p, miR-324-3p and miR-139-3p whose overexpression modulates several genes associated with a wide range of heart functions as cell stress, metabolism, cell survival and apoptosis. [score:6]
Interestingly, cells pretreatment with PD 098059 prevented Ucn-1 upregulation of miR-125a-3p (Fig.   4A) and miR-324-3p (Fig.   4B), but it did not affect miR-139-3p (Fig.   4C) expression levels during cells reperfusion. [score:6]
Our data indicates that the upregulation of miR-125a-3p in cardiac myocytes changed significantly the expression of different genes whose functions are associated with cell stress, metabolism, or cell survival and apoptosis. [score:6]
Furthermore, Epac2 specific inhibition with ESI-05 (10 μM) [16], blocked the effect of Ucn-1 on miR-324-3p (Fig.   4B) and miR-139-3p (Fig.   4C) regulation, but not miR-125a-3p expression (Fig.   4A). [score:6]
Ucn-1 inverted the effect of I/R and enhanced the expression of miR-125a-3p and miR-324-3p, meanwhile it decreased miR-139-3p expression. [score:5]
We found that, after I/R, the expression of miR-125a-3p (Fig.   4A) and miR-324-3p (Fig.   4B) decreased, whereas the expression of miR-139-3p increased (Fig.   4C). [score:5]
Figure  5D and E shows that the expression of miR-125a-3p and miR-324-3p was downregulated in I/R group as compared to Sham. [score:5]
Bar graphs show rate changes of genes mRNA expression assessed by qRT-PCR in neonatal rat cardiomyocytes infected with lentivirus overexpressing miR-125a-3p (A), 139-3p-3p (B) and miR-324-3p (C). [score:5]
Furthermore, we observed that overexpression of miR-125a-3p inhibited others genes, as TAZ, CPT2 and MTFR1, related to mitochondria remo deling and metabolism. [score:5]
In addition, we found that the incubation of cardiac myocytes with 8CPT (10 μM), specific agonist of Epac1 and 2 [16], mimicked mostly the effect of Ucn-1. The administration of 8CPT prevented I/R -induced changes on the expression of miR-324-3p and miR-139-3p; meanwhile it did not affect the change induced by I/R of miR-125a-3p expression. [score:5]
Figure 3Urocortin-1 regulates miR-125a-3p, miR-324-3p and miR-139-3p expression in isolated cardiac myocytes. [score:4]
Previous reports demonstrated that circulating miR-125a-5p was associated with heart failure [29], and it was significantly upregulated in early phase of reperfusion in mice [30]. [score:4]
In the current study, we demonstrated that the addition of Ucn-1 or Ucn-2 in the beginning of reperfusion changed the expression of miR-125a-3p, miR-324-3p, and miR-139-3p in different experimental mo dels of I/R. [score:3]
Figure  3 shows that the expression of miR-125a-3p and miR-324 are increased significantly upon treatment with Ucn-1. In contrast, the level of miR-139-3p did not change significantly in cardiac myocytes incubated with any of the used Ucn-1 doses. [score:3]
To ensure miRNAs mimics cells delivery, Lentivirus -expressing miR-125a-3p (LV-miR-125a-3p), Lentivirus-miR-139-3p (LV-miR-139-3p) and Lentivirus-miR-324-3p (LV-miR-324-3p) were constructed by cloning the pre-microRNA sequence in plasmid (pSIN-DUAL-GFP). [score:3]
Ucn-2 infusion partially recovered the levels of miR-125a-3p (Fig.   5D); meanwhile, it reverted significantly the expression of miR-324-3p (Fig.   5E). [score:3]
These data reveal that Ucn-1, through miR-125a-3p, miR-324-3p and miR-139-3p, might target multiple genes involved in different signaling pathway implicated in cardioprotection, which will induce synergetic beneficial effects. [score:3]
To validate microarray results, we further examined the expression of miRNAs using qRT-PCR in samples from Langendorff-perfused hearts undergoing the same protocol as in Fig.   1. We focused on 6 miRNAs, miR-30c-2, miR-29a-3p, miR-125a-3p, miR-139-3p, miR-320, and miR-324-3p, which role in cardioprotection is still unknown. [score:3]
Bar graphs showing fold changes in the expression of miR-125a-3p (A), miR-324-3p (B) and miR-139-3p (C) in isolated cardiac myocytes treated 10 minutes with increasing concentrations of Ucn-1 (2, 10 and 50 nM). [score:3]
Similarly, Ucn-2 infusion in the animal mo del of I/R modulated the expression of miR-324-3p and miR-139-3p, but it failed to recover completely miR-125a-3p levels. [score:3]
Urocortin-1 modulates the expression of miR-125a-3p, miR-324-3p, and miR-139-3p in adult cardiac myocytes. [score:3]
Therefore, Ucn-2 was used at 150 µg/Kg to examine the expression of miR-125a-3p, miR-324-3p, and miR-139-3p in hearts’ samples taken 24 hours after surgery. [score:3]
miR-125a-3p also reduced significantly the expression of MAP3K12 and XBP1, genes associated with cell stress. [score:3]
Nevertheless, changes in the levels of miR-29a-3p, miR-30c-2, and miR-320 were not significantly affected by Ucn-1. To assess the endogenous expression of miR-125a-3p, miR-324-3p, and miR-139-3p, we treated isolated cardiac myocytes with different concentrations of Ucn-1 (2, 10 and 50 nM). [score:3]
Altogether, these data suggest that Ucn-1 applied on the onset of reperfusion regulates differentially miR-125a-3p, miR-324-3p and miR-139-3p through ERK1/2 and/or Epac2 signaling pathways. [score:2]
Moreover, Ucn-1 evoked changes in others genes regulated by miR-125a-3p, miR-324-3p and miR-139-3p were not significantly different (data not shown). [score:2]
Therefore, we examined the implication of ERK1/2 and Epac2 signaling pathway in Ucn-1 regulation of miR-125a-3p, miR-324-3p and miR-139-3p. [score:2]
The role of miR-125a-3p, miR-324-3p, and miR-139-3p in cardioprotection is still unclear. [score:1]
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3
[+] score: 154
For example, the predicted target genes of miR-125a-3p were found to be involved in some biological process including transmission of nerve impulse, regulation of action potential in neuron, regulation of inflammatory response, regulation of gene expression, synapse assembly, synaptic transmission, long-term synaptic potentiation, regulation of membrane potential, neuron fate commitment (Table 2). [score:9]
We detected the down-regulation of miR-125a-3p and up-regulation of p38 MAPK (mitogen-activated protein kinase) and CGRP (calcitonin gene-related peptide) following the orofacial inflammatory pain. [score:7]
Kumar et al. [17] described the down-regulation of miR-125a-3p expression was involved in West Nile virus -induced neuroinflammation in mice brain by regulating some anti-viral cytokines. [score:7]
Candida albicans and lipopolysaccharide (LPS) -induced inflammation up-regulated miR-125a expression in macrophages and the pri-miR-125a transcription was also regulated by MAPK signal pathway [31]. [score:7]
Conversely, p38 MAPK mRNA expression was significantly increased in a dose -dependent manner when miR-125a-3p inhibitor was transfected into ND8/34 cells compared with the non-target control (p<0.01) (Figure 4B). [score:6]
Furthermore, we focused on a down-regulated miRNA, miR-125a-3p, and found a negative relationship between miR-125a-3p and p38 MAPK expression. [score:6]
Furthermore, GO analysis indicated miR-125a-3p was involved in some processes of pain transduction including transmission of nerve impulse, synaptic transmission, regulation of action potential in neuron, regulation of inflammatory response and regulation of gene expression, which reminds us to pay more attention to it. [score:6]
The pain induced a decreased miR-125a-3p expression and increased p38 MAPK expression in vivo. [score:5]
The results showed that overexpression of miR-125a-3p significantly diminished luciferase activity (decrease ∼35% at 25 nM, and ∼55% at 50 nM of miR-125a-3p mimic, respectively, p<0.01), while the miR-125a-3p inhibitor increased the luciferase activity (increase ∼20% at 25 nM, and ∼40% at 50 nM of miR-125a-3p, p<0.05 and p<0.01, respectively), both in a dose -dependent manner. [score:5]
Changes of p38 MAPK mRNA expression following over -expression of miR-125a-3p in ND8/34 cells. [score:5]
Correlation of miR-125a-3p Expression with the Head Withdrawal Threshold, p38 MAPK and CGRP mRNA Expression in Rat TGs. [score:5]
Pearson correlation analysis was used to analyze the correlations of miR-125a-3p expression with p38 MAPK, CGRP mRNA expression and head withdrawal threshold. [score:5]
They were transfected with 0.5 µg pMIR-p38 MAPK 3′UTR-wt or pMIR-p38 MAPK 3′UTR-mt and 50 nM miR-125a-3p mimic, inhibitor or non-target control (Life Technology, NY, USA), and 0.05 µg of the Renilla luciferase vector pRL-TK (Promega, CA, USA) for normalization. [score:5]
Our result also showed that down-regulation of miR-125a-3p significantly increased MAPK mRNA level in vitro, and luciferase assay confirmed a direct binding of miR-125a-3p to the 3′UTR of p38 MAPK mRNA. [score:4]
In order to determine whether miR-125a-3p plays a role in regulating p38 MAPK expression, we first aligned the miR-125a-3p sequence with p38 MAPK 3′UTR on the website (http://www. [score:4]
Compared with non-target control, the expression of p38 MAPK mRNA was significantly decreased at 48 h after miR-125a-3p mimic transfection (p<0.01). [score:4]
ND8/34 cells were transfected with 0, 25, 50 nM of miR-125a-3p mimic or inhibitor (Life Technolgoy, NY, USA) using Lipofectamine 2000 transfection reagent (Invitrogen) according to the manufacturer's instructions. [score:3]
We detected the level of p38 MAPK level at different time points and analyzed the correlation of miR-125a-3p level with p38 MAPK, CGRP mRNA expression and the head withdrawal threshold. [score:3]
The Pearson correlation analysis indicated that miR-125a-3p expression level was positively correlated with the head withdrawal threshold (R = 0.731, p<0.001) and negatively related to p38 MAPK and CGRP mRNA level (R = −0.673 and −0.699, respectively, p<0.001). [score:3]
The differential expression way was also observed in miR-125a. [score:3]
Expression of miR-125a-3p, p38 MAPK and CGRP mRNA in Rat TGs. [score:3]
Finally, we detected whether p38 MAPK was the direct target of miR-125a-3p using luciferase assay. [score:3]
Some studies showed increased miR-125a expression [18], [19], [31] and whereas others did not [17]. [score:3]
The present study indicated a decreased miR-125a-3p expression. [score:3]
MiR-125a-3p negatively regulated the p38 MAPK expression in ND8/34 cells. [score:3]
Luciferase assay indicated p38 MAPK is the direct target of miR-125a-3p. [score:3]
Effects of miR-125a-3p on p38 MAPK expression and luciferase activity in ND8/34 cells. [score:3]
Besides, our study also indicates that miR-125a-3p might have a negative correlation with the development and maintenance of inflammatory pain via regulating the p38 MAPK signaling. [score:3]
Expression of miR-125a-3p (A), CGRP (B) and p38 MAPK (C) mRNA in ipsilateral TGs and head withdrawal thresholds (D) in ipsilateral orofacial region at different time points following CFA injection into rat orofacial skin. [score:3]
These results indicate that p38 MAPK gene is directly regulated by miR-125a-3p (Figure 4C). [score:3]
The inhibition of miR-125a-3p on p38 MAPK mRNA was dose -dependent. [score:3]
p38 MAPK mRNA levels after the transfection of miR-125a-3p non-target control with different doses (0, 25, 50 nM) had no significant changes. [score:3]
The sequences of forward and reverse primers are listed in Table 1. The relative expression of miR-125a-3p at different time points was detected as mentioned above. [score:2]
Compared with the baseline of normal control, the expression of miR-125a-3p after CFA injection decreased significantly from 12 h, attained the lowest level at 3 d, and then began to rise gradually at 5 d, but the decrease was still significant (p<0.01). [score:2]
The results indicated miR-125a-3p might be negatively correlated to the severity of inflammation and pain in orofacial region and might participate in the process of the development of inflammatory pain following CFA injection via the p38 MAPK signal pathways. [score:2]
Recently, emerging evidence showed miR-125 is involved in the regulation of cell stress, inflammation and pain. [score:2]
Based on these findings, we focused on miR-125a-3p and p38 MAPK, and hypothesized that miR-125a-3p could control CFA -induced orofacial inflammatory pain in TGs by regulating the activation of p38 MAPK signal pathway. [score:2]
0111594.g004 Figure 4(A) Binding sites alignment of the mature miR-125a-3p and the 3′UTR of rat p38 MAPK gene (left) and base pair difference between wild type (WT) and mutant type (MT) of p38 PAPK gene 3′ UTR (right). [score:1]
Other studies had focused on the relationship between miR-125 and p38 MAPK. [score:1]
Murata et al. [18] detected the increased plasma concentration of miR-125a-5p and suggested miR-125a-5p may be a potential diagnostic marker of rheumatoid arthritis. [score:1]
At 7 d, the miR-125a-3p level tended toward the baseline, and then returned to the baseline at 14 d (Figure 3A). [score:1]
Then we detected the p38 MAPK mRNA level in ND8/34 cells after miR-125a-3p transfection. [score:1]
We constructed the reporter plasmids containing 3′-UTR of p38 MAPK gene, as well as the mutant constructs with the potentially mutated miR-125a-3p binding sites. [score:1]
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4
[+] score: 88
Interestingly, miR-22, miR-1224 and miR-125-3p were initially up-regulated under EGF and bFGF treatment, but reversed their quantitative expression in the presence of IGF-1. In addition, miR-214 and miR-708 were expressed inconsistently in Group A while their expression went down in Group B. To validate the microRNA microarray expression data, a qRT-PCR assay was conducted to confirm the expression levels of three randomly selected microRNAs (let 7-b, miR-181a, and miR26a). [score:13]
Since the down-regulation of microRNAs may cause the up-regulation of targeted genes, we hypothesized that the presence of IGF-1 triggers the expression of certain genes by down -regulating key microRNAs (miR-1224, miR-125a-3p, miR-214, miR-22, miR-320, miR-708, and miR-93), which in turn enhance NPCs proliferation and survivability. [score:12]
Protein kinase B or Akt, a key protein involved in the activation of PI3K-Akt pathway and is crucial in promoting cell survivability [43], is inhibited by the key microRNAs (miR-22, miR-214, miR-125a-3p, miR-320 and let-7 family) that are down-regulated with the addition of IGF-1. Chen et al. reported that down-regulation of miR-133b significantly overexpressed Akt1 mRNA, which increased T24 bladder cancer cell proliferation and reduced cell apoptosis [44]. [score:11]
miR-93, a microRNA frequently associated with TGF-β signaling in controlling cell cycle arrest [26], cell proliferation, and differentiation [27], was also down-regulated in both Groups A and B. Moreover, we discovered that miR-1224 and miR-125a-3p, which were initially up-regulated in Group A, became down-regulated at day 3 and 5 in Group B post -induced with IGF-1. Both miR-1224 and miR-125a-3p play important roles in maintaining cell proliferation and survivability. [score:10]
The down-regulation of miR-125a-3p has been associated with a reduction in apoptosis by targeting p53 mRNA and an increase in cell proliferation and migration by up -regulating Fyn expression [31, 32]. [score:9]
However, BMSC-derived NPCs with addition of IGF-1 showed 12 microRNAs which include miR-22, miR-1224, miR-125a-3p, miR-214, miR-320, miR-708 and miR-93 were consistently down-regulated and only miR-496 remained up-regulated compared to Group C from Day 1 to Day 5. The let-7 family (let-7b, let-7c, let-7d, let-7e and let-7i) were constantly down-regulated in both groups. [score:9]
The genes up-regulated by down-regulation of miR-22 (A); miR-125a-3p (B); let-7 family (C); miR-214 (D); and miR-320 (E) were analyzed using GeneMANIA web tool with default weighting method (i. e., weighting based to maximize connectivity between input genes). [score:7]
MicroRNAs Query Genes miR-22 Myc; Ets1; Tp53; Agt; Esr1; Pten; Akt1 miR-214 Bcl2; Adora1; Myc; Neurod1; Dhcr24; Kras; Fgfr1; Apc; pcgfr1; Prnp; Akt1 miR-125a-3p Bcl2; Egfr; Tp53; Apc; Akt1; Rela miR-320 Bcl2; Adora1; Acvr1; Neurod1; Dhcr24; Tp53; Hmox1; Nol3; Pten; Akt1; Cebpb Let-7 Family Cdkn1a; Tnf; Bcl2; Adora1; Egfr; Myc; Il10; Acvr1; Sycp3; Neurod1; Dhcr24; Cdkn1b; SMAD3; Kras; ras3; Neurod1Birc2; Tp53; Kcnh8; FN1; Fgfr1; Clu; Fas; Pten; Akt1; Rela; Cebpb We assessed the predicted target genes of the down-regulated microRNAs with the KEGG database. [score:6]
These data support our findings that the down-regulation of mir-125-3p reduced apoptosis and increased cell proliferation possibly by a p53- and Fyn-regulated manner. [score:5]
Query genes for individual microRNA are listed in Table 5. The major targeted genes by all or four out of five key microRNAs (miR-22, miR-214, miR-125a-3p, miR-320 and let-7 family) included Akt1, Tp53, Pten and Bcl2. [score:3]
Ninio-Many L. Grossman H. Shomron N. Chuderland D. Shalgi R. MicroRNA-125a-3p reduces cell proliferation and migration by targeting Fyn J. Cell Sci. [score:2]
Jiang L. Chang J. Zhang Q. Sun L. Qiu X. MicroRNA hsa-miR-125a-3p activates p53 and induces apoptosis in lung cancer cells Cancer Investig. [score:1]
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5
[+] score: 26
We also looked at genes other than the ones differentially expressed in our gene array analysis Figure  5 and found that miR-125a targets many cell cycle genes, like Ccnd1, p21, and Cdk2, which may prove to be instrumental in unraveling the mechanism of parity -induced protection against breast cancer. [score:5]
Among the important genes were Lifr, Acvr1c, and Pparγ which were found to be targeted by microRNAs in our dataset like miR-143, miR-30, miR-140, miR-27b, miR-125a, miR-128ab, miR-342, miR-26ab, miR-181, miR-150, miR-23ab and miR-425. [score:3]
However, miR-125a-5p is the only microRNA that was found to target both Acvr1c and Lifr. [score:3]
It was found to be a putative target for let-7 family members, miR-26ab, miR-181 family, miR-150, miR-27b, miR-23ab, miR-425, miR-125a-5p, and miR-128ab. [score:3]
Previously, miR-125a-5p was also reported to target Lin28, which is again very interesting in the context of stem cells. [score:3]
It was found to be targeted by multiple microRNAs in our analysis, including miR-143, miR-30 family members, miR-140, miR-27b, miR-125a-5p, miR-128ab, and miR-342-3p. [score:3]
Down regulation of microRNAs, like miR-28, miR-125a, and miR-503, could possibly lead to up regulation of p21 in parous ALDH positive MECs. [score:3]
Furthermore, because these genes are regulated by miR-125a-5p, it is possible that miR-125a-5p plays a key regulatory role in putative stem cells of MECs and is involved in parity -induced protection against breast cancer. [score:3]
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6
[+] score: 21
More importantly, the miRNAs analyzed in this study not only included the miRNAs like Let-7a, miR-15b, miR24, miR-100 and miR-125 which may suppress the expression of cyclins A and B, and miRNAs such as Let-7a, miR24 and miR-125 which may regulate activity of CDK1, but also miRNAs such as miR-181a, miR-221 and miR-222 which can target CDK inhibitors [30– 32]. [score:10]
To investigate whether miRNAs have a role in the cell cycle regulation of splenocytes following aniline exposure, the expression of miRNAs, including Let-7a, miR-15b, miR24, miR-100, miR-125, miR-181a, miR-221 and miR-222 which are known to mainly control G2/M phase regulators [30– 32], was analyzed by using real-time PCR and the results are presented in Fig 7. Aniline exposure led to significantly decreased expression of Let-7a (decreased 82%), miR-15b (decreased 62%), miR24 (decreased 78%), miR-100 (decreased 63%), miR-125 (decreased 86%), whereas miR-181a, miR-221 and miR-222 increased by 155%, 78% and 56%, respectively, in comparison to controls (Fig 7). [score:5]
Real-time PCR analysis of miRNAs Let-7a, miR-15b, miR24, miR-100 and miR-125 (A), and miRNAs miR-181a, miR-221 and miR-222 (B) expression in rat spleens following aniline exposure. [score:3]
Therefore, greater decreases in Let-7a, miR-15b, miR24, miR-100 and miR-125 expression and significant increases in miR-181a, miR-221 and miR-222 levels in the spleens following aniline treatment may be mechanistically important in generalizing that aniline exposure leads to increased cyclin A, cyclin B, CDK1, and decreased p21, p27, thus triggering the splenocytes to go through G2/M transition. [score:3]
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7
[+] score: 19
Specifically, expression levels of pri-mir-9-1 (Figure 3d, black line, #) were significantly decreased at 8 weeks post OVX, while pri-mir-125a expression was decreased at 12 weeks post OVX (Figure 3g, black line, #). [score:5]
Experiment 1: Expression of E [2]-responsive mature miRNAs in the hypothalamus of ovarian intact animals changes with ageOur previous studies showed that E [2] regulated a subset of mature miRNAs (let-7i, miR-7a, miR-9, miR-9–3p, miR-125, miR-181a, and miR-495) in an age- and brain-region dependent manner [46]. [score:4]
First, we analyzed the expression levels of the primary transcripts, which demonstrated that both PPT and DPN treatment significantly decreased the expression of pri-miR-7a, pri-miR-125a, pri-miR-181a, and pri-miR-495 compared to either vehicle or E [2] treated animals (Figure 9a). [score:4]
miR-125a: Ovarian intact animals had significantly higher levels of miR-125a expression at 18 mo. [score:3]
Our previous studies showed that E [2] regulated a subset of mature miRNAs (let-7i, miR-7a, miR-9, miR-9–3p, miR-125, miR-181a, and miR-495) in an age- and brain-region dependent manner [46]. [score:2]
One way ANOVA analyses across the deprivation time points showed that pri-mir-7a-2, pri-mir-9-1, pri-mir-125a, pri-mir-181a, and pri-mir-495 were all significantly altered by OVX alone, and in general, they were all decreased with age (Figure 3, black line, #). [score:1]
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[+] score: 18
For example, a significant decrease in miR-125a-5p was seen following methamphetamine administration along with increased Ret mRNA expression, one of its purported targets. [score:5]
In general agreement with the array data, we observed a trend towards downregulation of miR-125-a-5p (p = 0.079, fold change −1.79) and miR-145 (p = 0.089, fold change −1.82) in methamphetamine self-administration rats (Figure  3a, n = 6 in each group). [score:4]
MiRNA candidates were selected based on novelty and mRNA targeting (miR-125a-5p, miR-145). [score:3]
We identified 78 miRNA and 150 mRNA transcripts that were differentially expressed (fdr adjusted p < 0.05, absolute log2 fold change >0.5); these included genes not previously associated with addiction (miR-125a-5p, miR-145 and Foxa1), loci encoding receptors related to drug addiction behaviors and genes with previously recognized roles in addiction such as miR-124, miR-181a, DAT and Ret. [score:3]
Validation experiments using qRTPCR showed a trend for miRNA-125a-5p and miR-145 in a consistent direction to the array data, however, this did not reach statistical significance. [score:2]
miR-125a-5p has not previously been implicated in addiction. [score:1]
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9
[+] score: 14
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-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-362, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, 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-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, 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-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, 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-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, 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-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
The relative expression intensities of miR-125 were 2.8 ± 1.6 in adenoma-free mice and 5.6 ± 2.7 in adenoma-bearing mice, thus accounting for a 2.0-fold upregulation. [score:6]
Our study showed that no miRNA was different between males and females in adenoma-free mice, while 3 miRNAs (miR-10a, miR-125, and miR-130a) were differentially expressed in adenoma-bearing male and female mice. [score:3]
The panels report the amplification curves for each one of the 20 mouse lung fragments tested, either adenoma-free (green) or adenoma-bearing (purple), relatively to miRNAs miR-125, miR-374, and miR-669k. [score:1]
According to volcano-plot analyses, no miRNA was different in males and females from adenoma-free mice, whereas 3 miRNAs (miR-10a, miR-125, and miR- 130a) from adenoma-bearing mice showed intergender differences. [score:1]
In particular, miR-10a is related to estrogen dependent cancer promotion [112, 113], miR-130a both to the estrogen and HER2 pathways [114, 115], and miR-125 to HER2/erbb2 estrogen sensitive oncogene activation [116, 117]. [score:1]
Validation of microarray data was performed by real time-qPCR for miR-125, miR-374, and miR-669k. [score:1]
Figure 4 The panels report the amplification curves for each one of the 20 mouse lung fragments tested, either adenoma-free (green) or adenoma-bearing (purple), relatively to miRNAs miR-125, miR-374, and miR-669k. [score:1]
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10
[+] score: 13
The presented data indicate that, among others, the activation takes place due to the opposed expression profile of genes and their regulating microRNAs at the site of inflammation (Figure 6); while the expression of all tested mesenchymal markers (Egr1, Fgf2, Fgf7, Jak2, Notch2, Hif1 α, Zeb2, Mmp9, Lox, and Vim) was significantly induced, microRNAs regulating their expression decreased (miR-192, miR-143, miR-375, miR-30a, miR-107, miR-200b, and miR-125a). [score:9]
Again, miR-125a, miR-30a, and miR-200b regulating Mmp9, Lox, and Vim, respectively [30– 32], are all downregulated in inflamed region as compared to uninflamed colon (Figures 3(e), 4(c), and 5(d)). [score:4]
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11
[+] score: 12
group C-C. Unbalanced perinatal metabolic environment and daily postnatal injection of pRLA have therefore different consequences on miR-125a-3p (constant expression vs. [score:3]
group C-C. Unbalanced perinatal metabolic environment and daily postnatal injection of pRLA have therefore different consequences on miR-125a-3p (constant expression vs. [score:3]
We previously reported a significant (p < 5.0E-2) expression difference of miR-125a-3p, −200a-3p, and −409-5p in the hypothalamus of male adult rats fed a HF-diet for their last 4 weeks of life (this study used the same C- and HF-diets than the ones used here) in relation to differences in their postnatal environment (Benoit et al., 2013). [score:3]
In our study, miR-125a-3p displayed similar expression between the four groups (padj-values > 1.2E-01 in all comparisons; see Supplemental Table S5). [score:3]
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12
[+] score: 11
Eight miRNAs, namely miR-125a-5p, -125b-5p, -126-3p, -210-3p, -494-3p, -21-5p, -29a-3p and -320a were significantly up-regulated in HF (vs. [score:4]
The up-regulation of these miRNAs in HF is supported by studies demonstrating that serum miR-125a-5p is significantly increased in human HF [3], and is one of the most abundant miRNA in pericardial fluid from HF patients undergoing open-heart surgery [37]. [score:4]
Validation of a selected few by qPCR identified 10 miRNAs - miR-133b-3p, miR-208b-3p, miR-21-5p, miR-125a-5p, miR-125b-5p, miR-126-3p, miR-210-3p, miR-29a-3p, miR-494-3p and miR-320a, that were significantly up-regulated in HF myocardium compared to normal controls. [score:3]
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13
[+] score: 9
MicroRNA-125 also promotes neuronal differentiation in human cells by repressing multiple targets (28) and in mammalian neurons, miR-125 is associated with regulation of dendritic spine length (29). [score:4]
By targeting glypican-4, miR-125 regulates cell growth (27). [score:4]
These include: let-7a, miR-124, miR-125a-5p, and miR-132. [score:1]
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14
[+] score: 9
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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, 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-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-99a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
Overexpression of miR-125a and miR-125b decreased ERBB2 and ERBB3 mRNA and protein levels, inhibited phosphorylation of ERK1/2 and AKT, and inhibited the anchorage-independent growth of ERα -negative/ErbB2 -overexpressing SKBR3 breast cancer cells [195]. [score:9]
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15
[+] score: 8
With the help of bioinformatics analysis, we filtered several miRNAs which were in the center of the miRNA-mRNA regulatory network and corresponding target genes, such as rno-miR-125a-5p. [score:4]
While these miRNAs which had higher degree were in the center of the network, such as rno-miR-125a-5p is the one that regulates the most genes, as many as 41 predicted target genes. [score:4]
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16
[+] score: 8
miR-21 and miR-125, which have been published to be androgen responsive and play a role in prostate carcinogenesis, are also upregulated in normal prostate [22], [23]. [score:4]
Studies to examine the dose- and time- dependent regulation of miR-214 and miR-125a, by androgens, are ongoing in our laboratories. [score:2]
Detection of miRs in serum miR-214 and miR-125a. [score:1]
However, only two miRs, miR-214 and miR-125a, positively correlated with androgen action in prostate. [score:1]
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17
[+] score: 7
Here, miR-125a-5p, miR-326, miR-345-5p, and miR-743b were downregulated in both intestinal tissue and intestinal T cells, while miR-17-1-3p, miR-290, and miR-3548 were upregulated (Figure 6E). [score:7]
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18
[+] score: 7
In Group 1, the most significantly up-regulated miRNAs were miR-1187, miR-125a-3p, miR-466c-5p, miR-5105 and miR-3472, whereas the most significantly down-regulated was miR-125b-5p. [score:7]
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19
[+] score: 7
In the mo del group, 17 miRNAs were downregulated, including miR-1, miR-133, miR-29, miR-126, miR-212, miR-499, miR-322, miR-378, and miR-30 family members, whereas the other 18 miRNAs were upregulated, including miR-21, miR-195, miR-155, miR-320, miR-125, miR-199, miR-214, miR-324, and miR-140 family members. [score:7]
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20
[+] score: 6
LncRNA MEG3 also was found to function as a ceRNA of several miRNAs, for instance, miR-125a-5p in immune thrombocytopenic purpura [13], miR-770-5p in Hirschsprung’s disease [22]. [score:3]
Li et al. [13] discovered that MEG3 repressed the expression of miR-125a-5p in immune thrombocytopenic purpura. [score:3]
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21
[+] score: 5
Emerging evidence indicates that miRNAs act as key modulators of target gene expression, and some, such as miR-21, miR-126, miR-33, miR-125, and miR-222, have been shown to be involved in the pathogenesis of stroke [5, 6]. [score:5]
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[+] score: 5
Other miRNAs from this paper: rno-mir-378a, rno-mir-378b
miR-378 binds to the 3′ untranslated region of VEGF to compete with miR-125a for the same seed region and strengthens VEGF expression [45]. [score:5]
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23
[+] score: 5
Importantly, the expression of hematopoiesis -associated miRNA (miR-451), brain-enriched miRNA (miR-143), hepatoblastoma -associated miRNA (miR-125) and of the short non-coding RNA RNU6 remained unchanged during the observed period (Fig. 6, lower row), indicating that the amount of these vesicle -associated miRNAs is not modulated at 2, 4 and 6 days after PHx. [score:3]
Other small non-coding RNAs included in the panel [i. e., RNU6, miR-143, miR-451 and miR-125 (close to significance, P = 0.057)] shows a constant expression throughout 2, 4 and 6 days after PHx and a trend of downr-egulation compared to the expression measured at day 0 (See Fig. 7, lower row). [score:2]
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[+] score: 4
Mol Endocrinol 35 Herrera BM Lockstone HE Taylor JM Wills QF Kaisaki PJ 2009 MicroRNA-125a is over-expressed in insulin target tissues in a spontaneous rat mo del of Type 2 Diabetes. [score:4]
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[+] score: 3
The deficiency of let-7 can stimulate DNA replication and cell division [27], so it suggested that let-7, miR-125, and miR-9 were the key regulators of retinal progenitor cells in the early to late developmental stages [28, 29]. [score:3]
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[+] score: 3
MiRNA-21 (A), miRNA-199a (B), miRNA-130b (C), miRNA-138-1 (D), miRNA-9 (E), miRNA-27a (F), miRNA-125a (G), and miRNA-320 (H) expression was not validated at 3 days after treatment with BM-MSC. [score:3]
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27
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
A few pri-miRNAs exhibit conservation along the entire length of the pri-miRNA (for example mir-497~195, mir-99b~let-7c~mir-125a, mir-124-2, mir-130a and mmu-mir-568) (Figure 10). [score:1]
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However, miR-125b-5p and BDNF are not uniquely expressed in RBCs, and further studies are therefore necessary to determine if miR-125-5p and BDNF are involved in other retinal remo deling processes. [score:3]
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Many of the best-studied miRNAs contained TFBS (e. g., mir-200a, b, c; mir-125a; let-7b), including those that have wide tissue expression patterns (e. g. mir-16-2) and others enriched in specific organs such as brain (mir-124-1,2) or liver (mir-122) [7]. [score:3]
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Similarly, longSAGE tags also suggest the expression of two human (mir-7-1 and mir-125a) and three mouse (mir-331, mir-351, and mir-495) miRNAs that have not been experimentally confirmed (Table 1). [score:3]
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Recent studies have successfully established a functional link between cell survival and a discrete group of survival -regulating miRNAs, including miRNA-1 [14], miRNA-125 [15], miRNA-206 [14], miRNA-210 [16, 17] and miRNA-708 [18]. [score:2]
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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-1, rno-mir-92a-2, rno-mir-96, rno-mir-100, rno-mir-101a, rno-mir-122, 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
Recently, we reported that SR-BI, which delivers the bulk of the cholesterol substrate for steroidogenesis, is regulated by two specific miRNAs, miRNA-125a and miRNA-455, in rat granulosa cells, a mo del mouse Leydig cell line and the rat adrenal gland [19]. [score:2]
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These include miR-7, miR-9, miR-124a, miR-125a/b, miR-181b/c and miR-99a/b. [score:1]
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Reference miRNAs (rno-miR-27b-3p, rno-miR-21-5p, rno-miR-151-3p, rno-miR-191a-5p, mmu-miR-351-5p, rno-miR-125a-5p, rno-miR-181a-5p) were selected using geNorm [6], and reached stability criteria. [score:1]
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Guo S. Lu J. Schlanger R. Zhang H. Wang J. Y. Fox M. C. Purton L. E. Fleming H. H. Cobb B. Merkenschlager M. Microrna mir-125a controls hematopoietic stem cell number Proc. [score:1]
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Other miRNAs from this paper: rno-mir-125b-1, rno-mir-125b-2
Upon neural differentiation, miR-125 as a key player in the molecular cascade that contributes to the irreversible commitment of pluripotent human stem cells to the neural lineage [10]. [score:1]
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[+] score: 1
We found four microRNAs (LET-7, MIR-100, MIR-125, and MIR-126) that could detect teratomas and had previously been associated with oncogenic transformations (Gu et al., 2015, Wu et al., 2015). [score:1]
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Brain-enriched miRNAs such as miR-9, miR-124a, miR-125, and numerous others are induced in primary neural tissues and differentiating primary neurons [20]– [22]. [score:1]
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For example, the miR-125 and let-7 microRNAs are dramatically induced at puparium formation, in tight temporal synchrony with the 20E primary-response E74A mRNA, but do so in a manner that is independent of either 20E or EcR [24]. [score:1]
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Other miRNAs from this paper: hsa-mir-125a, hsa-mir-126, rno-mir-126a, rno-mir-126b
Exosomes secreted by mesenchymal stem cells promote endothelial cell angiogenesis by transferring miR-125a. [score:1]
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One DEM (miR-125a-5p) exhibited only a sex effect. [score:1]
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Synthetic miR-125 was also taken up by the synaptosomes through a non-specific endocytic mechanism. [score:1]
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The TPM of tsp-miR-100-5p and tsp-miR-100-3p, tsp-miR-125-5p and tsp-miR-125-3p, tsp-miR-9-1-5p and tsp-miR-9-1-3p, tsp-miR-9-2-3p and tsp-miR-9-2-5p behaved in similar fashion (Fig. 4, Fig. 5A and Table S5). [score:1]
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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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, 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-96, rno-mir-99a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
These include rno-miR-195, rno-miR-125a-5p, rno-let-7a, rno-miR-16, rno-miR-30b-5p, rno-let-7c, rno-let-7b, rno-miR-125b-5p, rno-miR-221, rno-miR-222, rno-miR-26a, rno-miR-322, rno-miR-23a, rno-miR-191, rno-miR-30 family, rno-miR-21, rno-miR-126, rno-miR-23b, rno-miR-145 and rno-miR-494. [score:1]
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