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19 publications mentioning rno-mir-152

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-152. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 114
In the aorta of the SD rats, we confirmed that the miR-152 expression was down-regulated in the HF-diet group, and it can be up-regulated after 12-week treatment of SHXXT (n = 6; Fig. 6C). [score:9]
To prove that miR-152 can regulate ERα gene expression via the suppression of DNMT1, we transfected the miR-152 precursor or inhibitor into the LPS -treated HASMCs. [score:8]
These findings indicate that miR-152 indirectly up-regulated ERα expression through its binding to DNMT1. [score:7]
On the contrary, DNMT1 protein levels were increased and consequently ERα protein levels were down-regulated by miR-152 inhibitor at 72 h (100 nM). [score:6]
The present study showed that miR-152 can down regulate DNMT1 which in turn inhibits methylation in the promoter of the ERα gene leading to higher ERα expression. [score:6]
To further examine whether miR-152 influences HASMC phenotypes through the change of ERα expression, the cell proliferation and migration were assessed at 48 h and 72 h after transfecting miR-152 precursor or inhibitor into the cells. [score:5]
The results showed that the DNMT1 protein levels were reduced and consequently ERα protein levels were up-regulated by miR-152 precursor at 72 h (100 nM; Fig. 7A). [score:4]
The reduced miR-152 can lose an inhibitory effect on DNA methyltransferase, which contributes to hypermethylation of the ERα gene. [score:3]
However, DNA methylation at ERα was increased by miR-152 inhibitor. [score:3]
The reduced microRNA-152 can lose an inhibitory effect on DNA methyltransferase, which leads to hypermethylation of the ERα gene and a decrease of ERα level. [score:3]
LPS -treated HASMCs were transfected with miR-152 precursor/inhibitor (25 nM and 100 nM) and a negative control miR (NC miR, 100 nM). [score:3]
Among 1,087 surveyed miRNAs, the expression level of miR-152 was decreased by 2.3-fold when HASMCs were treated with LPS for 24 h (data not shown). [score:3]
To examine the effect of miR-152 on cell proliferation, HASMCs were transfected with the miR-152 precursor or inhibitor and then were incubated in microplates at 37°C with 5% CO [2] for 48 h and 72 h. After that 0.5 mg/ml of dimethyl-thiazol- diphenyltetrazoliumbromide (MTT; Sigma-Aldrich, MO, USA) was added into each well. [score:3]
Therefore, we identified that miR-152 has an anti-atherosclerotic effect via its effect on the increase of ERα expression. [score:3]
0030635.g007 Figure 7LPS -treated HASMCs were transfected with miR-152 precursor/inhibitor (25 nM and 100 nM) and a negative control miR (NC miR, 100 nM). [score:3]
Expression of miR-152 in LPS -treated HASMCs and the aorta of the Sprague-Dawley rats. [score:3]
miR-152 expression in LPS -treated HASMCs. [score:3]
On the contrary, SHXXT could restore microRNA-152, decrease DNMT1 and increase ERα expression in both cellular and animal studies. [score:3]
Statin had no effect on microRNA-152, DNMT1 or ERα expression. [score:3]
Again, statin did not have any effect on increasing miR-152 but SHXXT could enhance miR-152 expression. [score:3]
Subsequent real-time PCR experiment confirmed that LPS can decrease miR-152 expression at 48 h and 72 h (P = 0.0015 and 0.006; Fig. 6A). [score:3]
Previous studies on cancers [23], [24] reported that miR-152 can bind to the 3′ untranslated region (UTR) of DNMT1. [score:3]
A negative control miRNA (#17110), hsa-miR-152 precursor (Product ID: PM12269) and hsa-miR-152 inhibitor (Product ID: AM12269) were purchased from the Ambion Inc. [score:3]
We validated that microRNA-152 can knock down DNMT1 in HASMCs leading to hypermethylation of the ERα gene. [score:2]
miR-152 regulates DNMT1 and ERα at the protein levels. [score:2]
microRNA-152 was found to be down regulated in the LPS -treated HASMCs. [score:2]
The DNMT family can be regulated by several miRs such as miR-29b, miR-148a and miR-152 [23]– [25], [27]. [score:2]
The results demonstrated that the transfected miR-152 precursor resulted in a concentration -dependent reduction of cell proliferation in the LPS -treated HASMCs at 48 h and 72 h (Fig. 7C; P<0.01). [score:1]
In conclusion, the present study showed that the level of miR-152 decreases under the pro-atherosclerotic stimulations. [score:1]
These results also suggested that miR-152 has an anti-atherosclerotic effect by decreasing cell proliferation. [score:1]
Gain and loss functions of ERα by miR-152. [score:1]
MSP analysis also showed that DNA methylation at ERα was reduced by miR-152 precursor in the LPS -treated cells (Fig. 7B). [score:1]
The effect of miR-152 on HASMC proliferation and migration. [score:1]
However, miR-152 did not influence HASMC migration at 48 or 72 h (data not shown). [score:1]
Accordingly, we speculated that miR-152 may be involved in DNMT1 -associated DNA methylation in the cardiovascular system. [score:1]
The present study showed that microRNA-152 decreases under the pro-atherosclerotic conditions. [score:1]
Furthermore, our cellular studies showed that miR-152 levels can be induced by SHXXT in a dose -dependent manner, but cannot be induced by simvastatin for 48 h or 72 h (Fig. 6B). [score:1]
0030635.g006 Figure 6(A) The miR-152 levels in the LPS -treated HASMCs were examined by real-time quantitative PCR and normalized to RU6B after 48 h and 72 h treatment with/without SHXXT. [score:1]
Therefore, we demonstrated a consistent change between DNMT1 and ERα methylation by the change of miR-152 levels. [score:1]
Unfortunately, we did have available human samples to compare miR-152 concentrations between atherosclerotic and non-atherosclerotic tissues. [score:1]
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[+] score: 106
Other miRNAs from this paper: rno-mir-130a, rno-mir-130b, rno-mir-132, rno-mir-184, rno-mir-212
Another line of reasoning is that miR-152 may target genes that require cytosolic ATP such that downregulation of these targets will result in eventual accumulation of cytosolic ATP concentration as observed in the OE152 cells. [score:8]
For this reason, we hypothesize that overexpression of miR-152, aside from targeting proteins required for ATP-generation such as Pdha1 and Gck, they may also target genes that require ATP in fundamental cellular processes in the beta cell. [score:7]
Concerning the miRNAs studied here, we previously showed that miR-130a expression is downregulated with increased glucose concentration in Wistar rat islets 10, which was supported by our findings in INS-1 832/13 cells for miR-130a, miR-130b and miR-152 (Supplementary Fig. S2). [score:6]
The transient modulation of miR-130a, miR-130b, or miR-152 in INS-1 832/13 cells by either over -expression or knock-down resulted in reciprocal effects on GSIS, but not KCl -induced insulin secretion agrees with targets primarily involved in modulating the cytosolic ATP concentration. [score:6]
These results provide strong evidence that at least miR-152 via AGO2 association, directly targets Pdha1 resulting in both reduced transcript and protein expression levels. [score:6]
The striking resemblance of ATP concentration changes during GSIS, and after inhibition of ATP synthase (oligomycin treatment) between OE152 cells and PDHA1 KD cells lend strong support to direct miR-152 mediated regulation of PDHA1. [score:5]
Previous reports regarding decreased glucokinase (GCK) mRNA expression in the pancreatic islets of T2D humans 30 and GK rats 31, and deficiency of pyruvate dehydrogenase activity 17 in the pancreatic islets of diabetic GK rats led us to focus on the potential targeting of miR-130a/b and miR-152 within the 3′UTR and coding sequence (CDS) regions of GCK/Gck and PDHA1/Pdha1 in human/rat (Supplementary Table 2). [score:5]
When miR-130a and miR-152 in combination were each overexpressed at half the amount of final concentration than when each miRNA was overexpressed separately, similar magnitude of reduction was observed for GSIS and insulin content, demonstrating the additive effect of miR-152 and miR-130a. [score:5]
Over -expression and co -expression of miR-152, miR-130a, and miR-130b in pancreatic islets. [score:5]
Additionally, we also observed reduced Gck expression both in the mRNA and protein levels, upon miR-152 overexpression (Fig. 4A,B). [score:5]
Moreover, despite different chromosomal locations of the three miRNAs in the human genome (chr11/miR-130a; chr22/miR-130b; chr17/miR-152), there was a notable co -expression among them, indicating highly-coordinated transcriptional regulation of these miRNAs in the human pancreatic islets (Fig. 1C). [score:4]
Of note, the miR-152 and miR-130a are among the 24 miRNAs we previously showed to be upregulated in the pancreatic islets of GK rats 10. [score:4]
Upregulation of miR-152, miR-130a and miR-130b in GK rat islets, and in human islets from donors with impaired glucose tolerance and type-2 diabetes. [score:4]
We previously determined that miR-152 and miR-130a were among the 24 upregulated miRNAs in the islets of the T2D mo del GK rat, compared to those of Wistar controls using a locked nucleic acid (LNA) -based miRNA array profiling approach 10. [score:3]
Specific primers and probes from TaqMan [®] MiRNA Assays (Applied Biosystems, CA, USA) were used to measure the expression levels of miR-130a-3p (#TM_000454), miR-130b-3p (#TM_000456), miR-152-3p (#TM_ 000475) and mRNA expression of their targets: Rat Pdha1 (Rn01424346_m1), Rat Gck (Rn00561265_m1), Human PDHA1 (Hs01049345_g1), and Human GCK (Hs01564555_m1). [score:3]
Among the 172 ATP -binding genes with unique putative miR-152 binding sites are the highly expressed adenylyl cyclase in the pancreatic islets, Adcy5 and Adcy6, involved in the conversion of ATP to cAMP 33 and two Na [+]/K [+] ATPase transporting subunit genes (Atp1a2 and Atp1a3) involved in establishing and maintaining the electrochemical gradients of Na [+] and K [+] ions across the plasma membrane. [score:3]
To conclude, we could show that miR-130a, miR-130b and miR-152 influence the metabolic control of GSIS via modulation of ATP levels, partially through targeting of PDHA1 and GCK in the pancreatic beta cell (Fig. 7). [score:3]
html) 29 to identify putative targets of miR-130a-3p, miR-130b-3p, and miR-152-3p. [score:3]
How to cite this article: Ofori, J. K. et al. Elevated miR-130a/miR130b/miR-152 expression reduces intracellular ATP levels in the pancreatic beta cell. [score:3]
We found that miR-130a, miR-130b and miR-152 or combination of miR-130a/miR-152 resulted in significant decrease in the expression of Pdha1 both in the mRNA and protein levels (Fig. 4A,B). [score:3]
Indeed, when we performed gene ontology (GO) enrichment on predicted targets unique to miR-152, we saw significant enrichment for the gene ontology molecular function category called “ATP -binding” (Benjamini corrected p-value = 0.013). [score:3]
To summarize, the similar beta cell functional deficiencies observed between the OE152 cells and PDHA1 KD cells, support the miR-152- mediated control of GSIS at the level of cellular metabolism via the negative regulation of PDHA1. [score:2]
Subsequently, we could show negative regulatory effects of miR-130a and miR-130b on glucokinase and PDHA1, and the direct biochemical interaction of miR-152, with Pdha1 mRNA using the AGO2 RIP assay. [score:2]
Hypothetically, LNAs that knock down miR-130a/miR-130b/miR-152 would affect the glucose conversion pathway in the mitochondria and assist in stabilizing the intracellular ATP to an optimal level. [score:2]
To determine enriched Gene Ontology categories for genes with unique putative binding sites for either miR-130a/b or miR-152, we used the Database for Annotation, Visualization and Integrated Discovery (DAVID) v6.7 web server (https://david-d. ncifcrf. [score:1]
Effect of modulating miR-130a, miR-130b, and miR-152 levels on insulin secretion in INS-1 832/13 cells. [score:1]
In this study, we showed that islets from hyperglycaemic human donors contain elevated levels of miR-130a, miR-130b and miR-152. [score:1]
For instance, we could observe that miR-152 impacted less on the ATP:ADP ratios during GSIS than either miR-130a or miR-130b. [score:1]
In cells transfected with combined Pre-miR-152 and Pre-miR-130a, the concentration of each Pre-miR was reduced to 25 nM. [score:1]
The characteristics of human pancreatic islet donors are in Supplementary Table 1. We found that the levels of miR-152, miR-130a and miR-130b were upregulated in the islets of hyperglycaemic donors (IGT/T2D) compared to those of normoglycemic (NGT) donors (Fig. 1B). [score:1]
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[+] score: 61
Although the suppression of cell apoptosis induced by miR-152-3p upregulation was not significant (p = 0.056), miR-152-3p inhibition significantly reduced cell viability (p < 0.01) and increased rates of apoptosis and necrosis, which supports an anti-apoptotic effect of miR-152-3p (Figure 4I). [score:8]
Additionally, pro-apoptotic genes including Caspase-3 and Faslg were inhibited by upregulation of miR-152-3p (Figure 4J). [score:6]
miR-152-3p directly targeted Atg12 and activated the anti-apoptotic gene Bcl-2, thus attenuating hypoxia -induced H9c2 cells apoptosis [41]; simultaneously, let-7i-5p played an anti-apoptotic role by inhibiting Faslg and, thus, attenuating the cell death-inducing signalling cascade [42, 43]. [score:6]
This indicates that miR-152-3p inhibited Atg12 expression by binding the 3′-UTR. [score:5]
To explore the mechanism through which miR-152-3p and let-7i-5p mitigate hypoxia -induced H9c2 cells apoptosis, we predicted potential targets of miR-152-3p and let-7i-5p based on TargetScan and RNA hybrid analyses [39, 40]. [score:5]
Upregulation of miR-152-3p significantly repressed luciferase activity in HeLa cells transfected with the wild-type Atg12 3′-UTR reporter (0.74-fold change, p = 0.017; Figure 5D), whereas this repression was completely abolished when the miR-152-3p binding site in Atg12 was mutated. [score:4]
Atg12 and Faslg Are Targets of miR-152-3p and Let-7i-5p, Respectively. [score:3]
These results demonstrate that miR-152-3p and let-7i-5p resemble miR-21-5p and miR-378-3p, which are highly expressed in hypoxic H9c2 cells-derived exosomes, and have anti-apoptotic and pro-viability effects in H9c2 cells under hypoxic stress. [score:3]
Additionally, we identified Atg12 and Faslg as the respective targets of miR-152-3p and let-7i-5p, which partly elucidates the anti-apoptotic mechanism of hypoxia -induced exosomal miRNA. [score:3]
Atg12 and Faslg mRNA levels were reduced when miR-152-3p and let-7i-5p were overexpressed in hypoxic H9c2 cells (Figure 5A,B). [score:3]
Atg12 and Faslg were predicted as putative targets of miR-152-3p and let-7i-5p, respectively. [score:3]
These results indicate that Atg12 and Faslg are the respective targets of miR-152-3p and let-7i-5p. [score:3]
To further investigate the biological function of hypoxia -induced exosomal miRNAs in H9c2 cell apoptosis, we selected miR-21-5p, miR-378-3p, miR-152-3p, and let-7i-5p, which were significantly upregulated in hypoxic exosomes and participated in apoptosis, for functional verification. [score:2]
Interestingly, we found that some exosomal DE miRNAs, including miR-21-5p, miR-378-3p, miR-152-3p, and let-7i-5p, had potential anti-apoptotic and pro-viability effects in H9c2 cells under hypoxic stress. [score:1]
Based on our small RNA-seq results and bioinformatic prediction, we selected several miRNA to use to verify function, including miR-21-5p, miR-378-3p, miR-152-3p, and miR-let-7i-5p. [score:1]
We constructed a dual luciferase report plasmid (pmirGLO- Atg12 3′-UTR) encoding the rat Atg12 3′-UTR that contains miR-152-3p binding sites. [score:1]
Based on these findings, we focused on miR-152-3p and let-7i-5p for further study. [score:1]
Bioinformatic prediction suggested that the 3′-UTR of Atg12 mRNA has one unique putative binding site for the miR-152-3p seed sequence (Figure 5C). [score:1]
More specifically, we demonstrated for the first time that miR-152-3p and let-7i-5p, which were enriched in exosomes derived from H9c2 cells under hypoxic conditions, played an anti-apoptotic role via the mitochondrial (intrinsic) and the death receptor (extrinsic) pathways, respectively. [score:1]
We found that miR-152-3p attenuated the reduction in cell viability (p < 0.01) and the increase in cell membrane damage (p < 0.05) induced by hypoxia in H9c2 cells (Figure 4G,H). [score:1]
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[+] score: 29
The results demonstrated that in the hypertonic dialysate group, miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were all significantly down-regulated whereas miR-122 was highly up-regulated (all P <0.05) (Figure  3). [score:7]
The miRNA screen identified 8 significantly down-regulated miRNAs (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b) and one highly up-regulated miRNA (miR-122) in the hypertonic dialysate group. [score:7]
It was found that 8 miRNAs were significantly and consistently down-regulated in the hypertonic dialysate group (miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b), and within which miR-192, miR-194 and miR-200b were also down-regulated in the normal saline group (Table  3). [score:7]
Compared with the control and saline groups, both miRNA microarray and real-time PCR analyses demonstrated that miR-31, miR-93, miR-100, miR-152, miR-497, miR-192, miR-194 and miR-200b were significantly down-regulated, and miR-122 was highly up-regulated in the hypertonic dialysate group. [score:6]
Several studies have demonstrated that miR-100, miR-152 and miR-497 are associated with the development of tumor and tumor metastasis [54- 56]. [score:2]
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[+] score: 17
The miRNAs with the most consistent female-biased expression were miR-29b (Fig.   3) and miR-152 (Fig.   3 and Fig.   4) with both showing an approximate 2-fold higher expression in females than males at 15, 21, 52, and 78 weeks of age. [score:5]
Female-biased expression of miR-29b and miR-152 occurred from 15 to 78 weeks of age while male-biased expression of miR-125b-5p and miR-99a occurred during this same age span. [score:5]
Despite only seven sexually dimorphic miRNAs being in common between the adult and the old rats (miR-125b-5p, miR-152, miR-29b, miR-374, miR-96, miR-99a*, and miR-99a), 91% (74/81) of the mRNA targets in the old rats were also mRNA targets in the adult rats. [score:5]
miR-152 is dysregulated in rat mo dels of NAFLD [60] and has been characterized to act as a tumor suppressor [61]. [score:2]
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[+] score: 12
There are also a number of miRNAs such as miR-132, miR-212, miR-130a and miR-152 shown to be upregulated in the pancreatic islets of the wi dely-studied T2D mo del Goto-Kakizaki rats (Esguerra et al., 2011) with active roles in beta cell stimulus-secretion coupling (Malm et al., 2016; Ofori et al., 2017). [score:4]
Expression of miR-200a, miR-130a and miR-152 in INS-1 832/13 cells (A–C) or in EndoC-βH1 cells (D–F) at different confluences. [score:3]
For miR-200a, miR-130a and miR-152, the expression levels were found not to be influenced by cellular confluence (Fig. S2). [score:3]
We also investigated the influence of confluence on the expression levels of miR-200a, miR-130a, miR-152, miR-132 and miR-212. [score:1]
The following primers from TaqMan [®] Gene Expression and TaqMan [®] miRNA Assays were used for qPCR: Cav1/CAV1 (Rn00755834_m1/Hs00971716_m1), Aifm1/AIFM1 (Rn00442540_m1/ Hs00377585_m1), miR-375 (TM_ 000564), miR-200a (TM_000502), miR-130a (TM_00454), miR-152 (TM_000475), miR-132 (TM_000457) and miR-212 (TM_002551) were used for qPCR. [score:1]
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[+] score: 8
Salvianolic acid B inhibits the Hh signaling pathway and reduces liver fibrosis by promoting the expression of miR-152 (Yu et al., 2015). [score:5]
Salvianolic acid B -induced microRNA-152 inhibits liver fibrosis by attenuating DNMT1 -mediated Patched1 methylation. [score:3]
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[+] score: 7
Down-regulation of Dicer1, predicted by miR-152, miR-203 and miR-222, could be a part of a complex regulation related to the global abundance of miRNAs and their requirements for processes such as cell-cycle exit control and onset of cell differentiation. [score:5]
Similar analysis of “late” group, including c-Maf, Ets1, N-Myc, Nfat5, and Nfib, yielded 10 miRNAs: miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351, with multiple connections. [score:1]
Ten miRNAs, miR-20b, miR-145, miR-152, miR-155, miR-181a, miR-203, miR-222, miR-301a, miR-324-5p, and miR-351. [score:1]
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[+] score: 7
Those miRNAs, we call them the epi-miRNAs, includes, for example, miR-148a, miR152, miR222 that targets mRNA of DNMTs and leads to re -expression of hyper-methylated tumor suppressors [32]. [score:7]
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[+] score: 6
On the contrary, other microRNAs identified by these authors, such as miR-152, miR-214, miR-206, and miR-221, either did not show significant expression changes or showed opposite behaviors in our analyses (such as the downregulation of miR-1). [score:6]
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[+] score: 6
miRNAs such as miR-133a, miR-185, miR-152, miR-34a and miR-342 which were reported to show increased expression were also up-regulated in our rat mo del. [score:6]
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[+] score: 5
Other miRNAs from this paper: mmu-mir-152
Several signaling pathways are participated in SalB's actions, e. g., Akt/mTOR/4EBP1, p38 mitogen-activated protein kinase (MAPK) /ATF2, and ERK1/2 signaling pathways, via up -regulating silent mating type information regulation 2 homolog 1 and inhibiting high mobility group box-1 protein, inducing microRNA-152 and attenuating DNA methyltransferase 1 -mediated Patched1 methylation, etc [5– 7]. [score:5]
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[+] score: 4
In this study, several altered hippocampal miRNA, including miR-133b, miR-152, miR-194, miR-22, miR-30a*, miR-347, and miR-874, have potential ability to regulate the expression of Gnai3. [score:4]
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[+] score: 3
6 was illustrated in Fig.   8B, including rno-mir-207, rno-mir-152, rno-mir-133a, may repress the expression of negative modulators, for example, Fads6, Samd14 and Fbxo46, respectively. [score:3]
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[+] score: 3
By contrast, miR-26b-5p, miR-199a-3p, miR-377–3p, miR-let-7f-5p, miR-200a-3p, miR-21–5p, miR-152–3p, and miR-192–5p expressions were repressed by SO diet consumption. [score:3]
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[+] score: 3
For instance, lower expression levels of miR-200b, miR-152 and miR-10a were associated with increased DNA methylation in bladder cancer [16], and miR-10a was silenced by aberrant DNA methylation in gastric cancer [17]. [score:3]
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[+] score: 2
Some of these miRNAs, i. e. rno-miR-34c, rno-miR-449a, rno-miR-301b, rno-miR-532-5p, rno-miR-219-5p, rno-miR-451, and rno-miR-152, were even 10-fold more abundant at E10 than at any other stages, providing a hint that these 7 miRNAs may play important roles in the regulation of progenitor cell proliferation. [score:2]
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[+] score: 2
In this context, previous studies have shown that lncRNA-XIST and miR-152 could interact with and repress each other and, in so doing, act as crucial regulators of the functions of human glioblastoma stem cells [16]. [score:2]
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[+] score: 2
Other miRNAs from this paper: rno-mir-21, rno-mir-96, rno-mir-193a, rno-mir-210, rno-mir-193b
Wu Y. Huang A. Li T. Su X. Ding H. Li H. Qin X. Hou L. Zhao Q. Ge X. Mir-152 reduces human umbilical vein endothelial cell proliferation and migration by targeting ADAM17FEBS. [score:2]
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