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20 publications mentioning rno-mir-137

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-137. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 73
Of the two miRNAs predicted to target EGR2, miR-19b was downregulated, which in accordance with the increased expression of EGR2, while miR-137 was downregulated only at T1 followed by upregulation from T2 to T4. [score:14]
Rno-miR-19a, rno-miR-19b-2 and rno-miR-214 were downregulated at all four time-points, while rno-miR-137 was downregulated at T1 followed by upregulation from T2 to T4 (Fig.   6). [score:10]
A previous study also demonstrated that miR-137 promotes proliferation and represses differentiation of NSCs by targeting Ezh2 [39] and regulates NSC maturation by targeting mind bomb-1 [40]. [score:6]
Rno-miR-19a (Rno, Rattus Norvegicus) and rno-miR-137, and their target gene EGR2, as well as rno-miR-19b-2 and rno-miR-214 and their target gene ARC were found to be closely related to neural developmental processes, including proliferation, differentiation, and maturation of NSCs. [score:6]
The expression of four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) and their target genes (EGR2 and ARC) were shown to be regulated by propofol in primary cultured embryonic NSCs. [score:6]
The results of the present study indicate that propofol may have the ability to regulate the expression of rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214 and their target genes, ARC and EGR2. [score:6]
Relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 at all four time-points (immediately (T1), Day 1 (T2), Day 3 (T3) and Day 7 (T4) after treatment with propofol or DMSO). [score:3]
The fold-change in the mean expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214 ranged from -2.56 to -12.15, -2.02 to 4.61, -2.33 to -6.68 and -2.16 to -4.63, respectively (Table  5). [score:3]
The expression patterns obtained in the present study combined with the results of these previous reports indicate that miR-19b and miR-137 interact with EGR2 to promote proliferation and repress the differentiation of NSCs. [score:3]
In this way, we confirmed two genes (EGR2 and ARC) and four miRNAs (rno-miR-19a, rno-miR-137, rno-miR-19b-2 and rno-miR-214) that exhibited at least a 2-fold change in the mean expression level following propofol treatment at all four time-points. [score:3]
Fig. 6Quantitative RT-PCR analysis of relative expression levels of rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214. [score:3]
Sun G Ye P Murai K Lang MF Li S Zhang H Li W Fu C Yin J Wang A miR-137 forms a regulatory loop with nuclear receptor TLX and LSD1 in neural stem cells. [score:2]
However, the potential relationship between EGR2 and miR-19b/miR-137 on the development of NSCs remains to be fully elucidated. [score:2]
Shi et al. found that miR-137 exerts a negative effect on proliferation of embryonic NSCs and then accelerates differentiation via a feedback regulatory loop with TLX and LSD1 [38]. [score:2]
MiR-137, miR-124, miR-34a, and miR-34c have also been implicated in ketamine -induced neurotoxicity in various in vivo and in vitro mo dels [20– 23]. [score:1]
MiR-137 is a versatile miRNA that plays different roles in the proliferation, differentiation and maturation of NSCs. [score:1]
MiR-124 and miR-137 affect early neurogenic response through cooperative control of caspase-3 activity [13]. [score:1]
The miRNAs predicted by all four databases (rno-miR-19b-2, rno-miR-137, rno-miR-19a and rno-miR-214, (Rno, Rattus Norvegicus)) were selected for validation (Table  4 and Fig.   5). [score:1]
[1 to 20 of 18 sentences]
[+] score: 59
The brain-specific miR-134 regulates dendritic spine development by repressing the translation of an mRNA encoding a protein kinase, Limk1, that controls spine development [21], while the brain-enriched miR-137 has a significant role in neuronal maturation and dendritic morphogenesis via direct targeting of Mib1, a ubiquitin ligase important for neurogenesis and neurodevelopment [22]. [score:10]
Another developmentally regulated miRNA is miR-137, with expression levels increasing more than four-fold in the telencephalon between E12 and E19. [score:5]
These were both targeted by miR-137, which appeared to have the greatest overall effect, whereas miR-212 had the least effect on these target gene constructs. [score:5]
This study confirmed the potency of miR-137 to down-regulate G-protein coupled receptor 88 (Gpr88) and wingless-type MMTV integration site family, member 7A (Wnt7a) using a reporter gene strategy. [score:4]
For example, miR-134 and miR-137 regulate neuronal maturation through the modulation of their target mRNA. [score:4]
Dysregulation of miR-137 has been associated with intellectual disability and Alzheimer’s Disease [51, 52] and the MIR137 gene has also recently found to be highly associated with schizophrenia in a genome wide screen and associated with cognitive function in patients with the disorder [53, 54]. [score:4]
Recent studies demonstrate increasing expression of miR-137 during neuronal differentiation, leading to reduced neural stem cell proliferation, accelerated neural differentiation and decreased dendritic development [22, 50]. [score:4]
Prominent among this group were miRNAs that are enriched in neurons and associated with developmental regulation (let-7i, let-7f, let-7b, miR-98), cell cycle regulation (miR-137, mIR-128) and neural activity (miR-132, miR-212). [score:4]
The only exception was the Plxnb2 construct, which displayed increased expression in the presence of synthetic miR-137. [score:3]
To generate reporter vectors bearing binding sites for the three miRNA examined in detail, miR-98, miR-212 and miR-137, oligonucleotides encoding target gene miRNA recognition elements (MREs) were annealed to form SpeI and HindIII restricted overhangs of a ligatable cassette compatible with SpeI and HindIII digested pMIR-REPORT vector (Ambion, Austin, TX) as described previously [69, 70]. [score:3]
Enriched ontologies of putative target genes of miR-98, miR-212 and miR-137 were identified using the DAVID online database. [score:3]
Microarray expression data was validated by RT-PCR for miR-98 (B), miR-212 (E) and miR-137 (H) with correlation coefficients of 0.64 (C), 0.62 (F) and 0.69 (I) respectively. [score:3]
In particular, regulation of 3’-UTR elements from Wnt7a (miR-137) and Gpr88 (miR-137) was particularly strong and, along with Clasp2 (miR-98) and Rab15 (miR-212) provides support for the role of post-transcriptional regulation in axon and dendritic growth, maturation and function [35– 38]. [score:3]
Figures show the normalised signal intensity values for miR-98 (A) and miR-212 (D) and miR-137 (G) at each developmental stage in the mesencephalon and telencephalon (*** = p < 0.001). [score:2]
Mir-137 is enriched in neurons and involved in neuronal maturation, regulation of dendritic development and phenotypic maturation of new neurons [22]. [score:2]
[1 to 20 of 15 sentences]
[+] score: 56
MiR-137 showed a trend of upregulation after 4 h post-OGD and continued to be upregulated as well at 6, 8 and 12 h. MiR-210 was upregulated after 6 h by >1.6-fold and significantly upregulated at 8, 12 and 24 h (p<0.05) suggesting a strong involvement of this miRNA in astrocytic response to ischemia (Figure 1). [score:13]
At 2 h, we saw a trend of upregulation of miR-29b in neurons that steadily increased up to 4-fold at 24 h. In contrast, in astrocytes, miR-29b showed a trend of upregulation later, after 6 h and a significant level increase by 2-fold only after 12 h. MiR-30b, miR-107 and miR-137 were uniquely upregulated only in astrocytes at different time-points, starting 6 h after OGD event. [score:10]
In this study, miR-137 was found to be a direct inhibitor of CDK6, suggesting a role of this miRNA in astrocytoma cell proliferation. [score:4]
In his study, Dharap [28] reported miR-29b (at 3, 6 and 24 h) and miR-137 (at 24 h) to be downregulated in a MCAo adult rat mo del, while Lei [33] reported the same findings in a TBI adult rat mo del at 6 h post injury. [score:4]
A direct comparison of expression levels of all the miRNAs used for our study between neurons and astrocytes undergoing OGD conditions, showed a significant difference at different time-points only for miR-29b, miR-30b, miR-107 and miR-137 (Figure 1). [score:4]
MiR-107, miR-30 and miR-137 were upregulated only in astrocytes. [score:4]
We screened the same miRNAs as described above (miR-21, miR-29b, miR-30b, miR-107, miR-137, miR-210) and found that IGF-I significantly decreases the expression of mir-29b in neurons. [score:3]
IGF-I did not have an effect on the expression levels of mir-21, mir-30b, mir-107, mir-137, or mir-210 in neurons. [score:3]
MiR-29b, miR-30b, miR-107 and miR-137 showed a significant difference in their expression levels between neurons and astrocytes undergoing OGD conditions (Figure 1). [score:3]
It has been reported that miR-137 expression is decreased in astrocytoma cell lines relative to normal brain tissues [76]. [score:3]
MiR-30b, miR-107 and miR-137 did not alter their expression levels in neurons. [score:3]
In light of these results, our findings that miR-137 level is increased only in astrocytes exposed to OGD-conditions, suggest that miR-137 may induce astrocytic proliferation as observed after ischemic stroke [77], [78]. [score:1]
We screened the same miRNAs as described above (miR-21, miR-29b, miR-30b, miR-107, miR-137, miR-210). [score:1]
[1 to 20 of 13 sentences]
[+] score: 39
Interestingly, PNM overexpression in B13 cells upregulated the expression of miR-137-3p, miR-135a-5p and miR-204-5p and repressed the expression of miR-210-3p to the same levels of those detected in rat islets, highlighting the potential role of these miRNAs in the reprogramming process. [score:10]
B13 cells that were transduced with Ad-PNM showed upregulation of 6 miRNAs (miR-134-5p, miR-455-3p, miR-384-5p, miR-137-3p, miR-135a-5p and miR-22-5p) and downregulation of 2 miRNAs (miR-335-3p and miR-148a-5p). [score:7]
The up-regulation of miR-455-3p, miR-137-3p and miR-135a-5p due to PNM expression observed in our panels (Table 3) was also validated in this single PCR study (Fig 6H–6J). [score:6]
Furthermore, expression levels of miR-137-3p, miR-135a-5p, miR-204-5p, miR-210-3p in reprogrammed B13 cells were consistent with the expression levels detected in rat islets and markedly differed from those displayed by rat exocrine tissue. [score:5]
To the best of our knowledge, there are no reports describing a link between β cell development or function and the remaining overexpressed miRNAs that were identified in the present study: miR-455-3p, miR-384-5p, miR-137-3p and miR-135a-5p. [score:4]
Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
Of note, using single qPCR assays we demonstrated that miR-455-3p, miR-137-3p and miR-135a-5p were expressed at very similar levels in reprogrammed B13 cells and pancreatic islets, suggesting a mechanistic relationship between these miRNAs and insulin production and/or β cell phenotype. [score:2]
0145116.g006 Fig 6Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
9 miRNAs were present in two categories; 5 of them were common between Tables 1 and 2 (miR-181a-5p, miR-204-5p and miR-2137, miR-421-3p and miR-483-3p), two miRNAs were present in both Tables 2 and 3 (miR-148a-5p and piR-335-3p) and the remaining two miRNAs were classified both in Tables 1 and 3 (miR-137-3p and miR-455-3p). [score:1]
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[+] score: 21
From P4 to P28, miRNAs displayed very similar expression between both progeny: 0–22 (<5%) miRNAs displayed differential expression and 0–7 of them (<2%) had expression differences higher than 3. Ratios of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p or miR-1843-5p expressions relatively to miR-124-3p expression calculated from RT-qPCR at P28 data matched those calculated from HTS data (Fig. 3B). [score:7]
Given the number of miRNAs and the limited quantity of material in individual ARC/MEs, we selected six miRNAs: miR-124a-3p which is wi dely expressed throughout brain 15, miR-29a/b-3p whose brain-specific knockdown results in neuronal cell death 16 17, miR-7a-5p and miR-137-3p which are expressed in hypothalamic nuclei including ARC 18, miR-24-3p and miR-1843-5p which are still poorly or not clearly documented. [score:6]
As the U6 snRNA was excluded from small RNA fractions and could not been used as an internal reference to quantify miRNA expressions, we quantified the expression of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p and miR-1843-5p relatively to that of miR-124-3p, at P4, P8, P14.4 and P21.4 relatively to P28, from RT-qPCR amplification or sequencing data (Fig. 3A). [score:5]
Expression of miR-7a-5p, miR-24-3p, miR-29-3p, miR-137-3p and miR-1843-5p were quantified relatively to those of miR-124-3p, and relatively to those of stage P28, by using the ΔΔCt method 25 and experimentally ascertained amplification efficiencies. [score:3]
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[+] score: 14
We conclude that miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543 represent an FGF2 -dependent system of multiple miRNAs that target specific genes operating in pathways and processes related to the lens differentiation (via c-Maf, Med1/PBP, N-myc, and Nfat5), miRNA-regulated RNA processing (via Cpsf6 and Tnrc6b) and nuclear/chromatin -based processes (via Med1/PBP, As1l, and Kdm5b/Jarid1b/Plu1). [score:4]
The current data suggest that multiple miRNAs, including miR-9, miR-137, miR-155, miR-301a, miR455, and miR-543 (Figure 7A and Figure 8A), regulate c-Maf expression through its 3′-UTR. [score:4]
We found that seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, target at least two “early” genes examined (i. e., c-Maf, N-Myc, and Nfib). [score:3]
Both c-Maf and Med1/PBP are predicted to be regulated by similar miRNAs, including miR-137, miR-200c, and miR-495 (Figure 7). [score:2]
Seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, and connections to specific functional groups of genes are shown. [score:1]
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[+] score: 10
Other miRNAs from this paper: hsa-mir-137
Although their particular role in aging remains to be established, two promising new targets involved in regulating degradation of damaged mitochondria are the micro RNA miR137 and the AAA ATPase p97. [score:4]
MicroRNA-137 is a novel hypoxia-responsive microRNA that inhibits mitophagy via regulation of two mitophagy receptors FUNDC1 and NIX. [score:3]
miR137 has been identified to inhibit mitophagy occurring in response to hypoxia, through reducing the interaction of LC3 with two mitophagy receptors, FUNDC1 and NIX (Li et al., 2014). [score:3]
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[+] score: 8
CaMKII, a target gene for miR-137 and miR-324-5p, is well-known for its role in synaptic plasticity. [score:3]
[63] A large number of cyclic AMP-specific PDEs are also targets of multiple miRNAs (miR-101a, miR-124, miR-721, miR-137, miR-19b, miR-30e, miR-365). [score:3]
For example, miR-218, miR-324-5p, miR-365 and miR-146a were localized on chromosome 10; miR-764-5p and miR-351 on chromosome X; miR-101 and miR-30e on chromosome 5; miR-582 and miR-137 on chromosome 2; miR-153 and miR-203 on chromosome 6; miR-124 and 181a on chromosome 3 and miR-135a*/miR-135a-3p and let-7i on chromosome 7. Some of the miRNAs that were localized on the chromosome and in close proximity showed the same direction of changes. [score:2]
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[+] score: 8
The expression levels of miR-376b-3p and miR-137-3p were downregulated, but miR-144-3p was upregulated on the 14th day compared to the 3rd day after injury (Figure  3C). [score:8]
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[+] score: 7
Consistently, a previous study showed that miR-137 regulates neuronal maturation by targeting the ubiquitin ligase Mib-1 [32]. [score:4]
At neonatal stage (around P0), when the majority of pyramid neurons have already migrated to their destinations and are extending axons and dendrites [31], we found high expression of several miRNAs at this stage, i. e. rno-miR-137 and rno-miR-19b. [score:3]
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[+] score: 5
Disagreements extend to other cell death-related microRNAs that were reported by Liu [6] to demonstrate changes in expression that we were not able to detect (mir-137 and miR-672) or whose expression did not seem to change in the present study (miR-214, miR-30-3p, miR-235-3p, and miR-674-5p). [score:5]
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[+] score: 5
Notably, a panel of 11 Runx2 -targeting miRNAs (miR-23a, miR-30c, miR-34c, miR-133a, miR-135a, miR-137, miR-204, miR-205, miR-217, miR-218, and miR-338) is expressed in a lineage-related pattern in mesenchymal cell types [20]. [score:5]
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[+] score: 5
Notably, cardiac-specific miR-1, miR-133, miR-208 and miR-499 were all suppressed by two or more orders of magnitude [34], [35], as were the stemness and cell cycle repressors miR-141 and miR-137 [36]; in contrast, the proliferative miRNAs, miR-222 [37], increased dramatically in MDCs, and miR-221 was undetectable in myocytes but highly expressed in MDCs (Figure 5D). [score:5]
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[+] score: 4
We found common expression of 9 miRNAs (miR-132, miR-137, miR-139, miR-29a, miR-324, miR-352, miR-282, miR-146a, and miR-23a) when our data were compared to a data set describing miRNA expression 60 d after pilocarpine -induced status epilepticus [24]. [score:4]
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[+] score: 4
Other miRNAs from this paper: rno-mir-132, rno-mir-212
The DPI treatment conspicuously increases miR-137 (Fig 3D) which was previously suggested to target Ezh2 [19, 20], the gene that encodes a histone methyltrasferase capable of catalyzing H3K27me2/3 modification as a component of the Polycomb Repressive Complex 2. However, Ezh2 mRNA is increased 3-fold by DPI (Fig 3C), suggesting that the miR-137- Ezh2 regulation is unlikely within the context of our experiment. [score:4]
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[+] score: 3
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-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, 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, miR-133b, miR-137, miR-155, and miR499 were exclusively expressed in the caudal region of the mouse epididymis but were wi dely distributed throughout the rat and/or human epididymis (S4 Table). [score:3]
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[+] score: 1
Among these miRNAs, miRNAlet-7a, miRNA-124, and miRNA-137 were reported to induce neuroprotection after cerebral ischemia, while miRNA-34a, microRNA-181c, and miRNA-17–92 were reported to exacerbates brain injury in ischemic Stroke (Szulwach et al., 2010; Liu et al., 2013; Hamzei Taj et al., 2016; Liang and Lou, 2016; Ma et al., 2016; Wang et al., 2016). [score:1]
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[+] score: 1
5 mmu-miR-214 -1.7 -6.1 -10.9 mmu-miR-137 -31.7 -6.8 -144.8 mmu-miR-29c -1.8 -10.5 -10.7 rno-miR-532–5p -2.0 -59.1 -126.9 mmu-miR-466d-3p -2.7 -4.2 -9.9 mmu-miR-466d-5p -23.2 -64.7 -105.7 mmu-miR-22 -1.6 -4.6 -9.9 mmu-miR-582–5p -21.3 -59.4 -97.1 mmu-miR-690 -1.9 -2.1 -9.7 rno-miR-421 -21.3 -59.3 -97.0 mmu-miR-193 -4.9 -3. 5 -8.1 mmu-miR-369–5p -20.9 -58.3 -95.3 mmu-miR-27b* -2.1 -2.9 -8.0 mmu-miR-684 -20.8 -58.1 -94.9 mmu-miR-378 -1.6 -4.6 -7.7 mmu-miR-375 -20.6 -57.6 -94.2 mmu-miR-9* -1.9 -18.4 -7.7 mmu-miR-337–5p -20.5 -57.4 -93.8 mmu-miR-204 -2.5 -5.3 -7.5 mmu-miR-15a* -20.3 -56.8 -92.8 mmu-miR-28* -1.9 -3.2 -6.5 mmu-miR-532–5p -19. [score:1]
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[+] score: 1
Similarly, Balaguer and colleagues noted that miR-137 was methylated in 81% of CRCs and while much less frequently seen in the histologically normal mucosa was ∼3 fold higher than in corresponding mucosa that was neoplasia-free [26]. [score:1]
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[+] score: 1
Shown are the Conserved TFBS and sno/miRNA tracks from the UCSC Genome Browser in the region corresponding to the small hairpin microRNA precursor encoding hsa-mir-137. [score:1]
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