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32 publications mentioning mmu-mir-376a

Open access articles that are associated with the species Mus musculus and mention the gene name mir-376a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 48
When compared with expression profiles of miRNAs associated with renal cancer, there was a 15% overlap with the miRNAs described in a recent report [54]; however, only miR-376a [67] out of the highly upregulated miRNAs, and miR-638, miR-200b and miR-200c from the highly downregulated miRNAs, were found to be in common between our studies and other studies [67], [70], [71], [72]. [score:8]
The double-stranded oligonucleotides encoding the pre-miRNA sequences of miR-376a, miR-299, miR-382 or irrelevant miRNA (a miR -negative control, predicted not to target any known vertebrate gene) were cloned into the pcDNA6.2-GW/EmGFP-miR expression vector such that the pre-miRNA insertion site was in the 3′ untranslated (3′UTR) region of the green fluorescent protein (GFP) gene as per the instruction manual (Invitrogen, Carlsbad, CA). [score:7]
0014416.g004 Figure 4 (A) of stably expressing miR-376a, miR376abc (a polycistronic cluster of miR-376a, miR-376b and miR-376c), miR-299-5p or miR -negative and 10-87 LP cells; (B) with stably expressing miR-376a, miR-376abc, miR-299-5p or miR -negative 10-87 HP cells. [score:5]
Indeed, the overexpression of miR-376a and the polycistronic cluster of miR-376a, miR-376b and miR-376c in non-invasive 10-87 LP cells were able to recapitulate the migration and invasion phenotypes of 10-87 HP cells. [score:3]
A human cytomegalovirus (HCMV) miRNA acts synergistically with a cellular miR-376a to suppress one of the major histocompatibility complex class I polypeptide-related sequences (MICB) during HCMV infection [47]. [score:3]
Recently, a target and function of miR-376a has been identified. [score:3]
We have identified miR-376a and the polycistronic miR-376abc as having a functional role in establishing the enhanced cell migration and cell invasion phenotypes, which are correlated with the expression of the VERO cell tumorigenic phenotype. [score:3]
To determine whether the overexpression of the identified signature miRNAs could confer phenotypic changes, stable cell lines were created by cloning the pre-miRNA sequences of miR-376a, miR-376abc, miR-299, or miR-382 into the pcDNA6.2-GW/EmGFP-miR vector, which contains a green fluorescent protein (GFP) cassette, and introducing them into the non-tumorigenic 10-87 LP cells. [score:3]
As found for 10-87 HP cells and 10-87 T cells, SF-VERO cells and A4497 VERO cells expressed increased levels of miR-376a, miR-654-3p, miR-543, and miR-382 over the levels found in pAGMK cells (Table 4). [score:3]
An expression plasmid for the polycistronic gene cluster for miR-376a, miR-376b and miR-376c was generated by amplifying 200 bp up-stream and 200 bp down-stream of the genes (termed as miR-376abc) in VERO cell DNA using primers 5′-CCCTCGACGAGAGTGATGGAAGGTGAATC-3′ and 5′-CCAGATCTATACTGAGAACACAGCCTTGT-3′. [score:2]
In agreement with the wound-healing assay, over -expression of miR-376a or miR-376abc also resulted in more than a four-fold increase in invasiveness, whereas miR-299 or miR-382 had no effect (Fig. 4B). [score:2]
The cells expressing miR-376a or miR-376abc displayed an increase in migration compared with control 10-87 LP cells. [score:2]
The following oligonucleotides were used to generate the pre-miRNAs: miR-376a sense, 5′-tgctGTAAAAGGTAGATTCTCCTTCTATGAGTACATTATTTATGATTAATCATAGAGGAAAATCCACGTTTTC-3′ and miR-376a anti-sense 5′- cctgGAAAACGTGGATTTTCCTCTATGATTAATCATAAATAATGTACTCATAGAAGGAGAATCTACCTTTTAC-3′. [score:1]
While the specific effect of miR-376a on tumorigenicity has not yet been demonstrated, it is plausible to suggest that the 10-87 VERO cells might use a similar mechanism as does HCMV to escape the immune system during tumor growth in athymic nude mice. [score:1]
These experiments demonstrated that miR-376a and miR-376abc were sufficient to confer the cell migration and invasion phenotype. [score:1]
qRT-PCR analysis confirmed that miR-376a, miR-654-3p, miR-543, miR-382, miR-31, miR-200c, miR-218, and miR-183 paralleled the microarray miRNA levels. [score:1]
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2
[+] score: 41
Figure 4. The ‘extended VCR’ of stratum 2 (shared by Homo and Pelodiscus sequences): (a) miR-16 target site (also shown in Fig. 2e) and nearby target sites for miR-376a, miR-335-3p, miR-493 and miR-379 (the Xenopus sequence contains a 44-bp insertion at the site of the asterisk that includes two target sites for miR-335-3p are shown in red); (b) conserved pair of target sites for miR-320a and miR-182; (c) conserved triplet of target sites for miR-378, miR-99a and miR-30a A notable feature of stratum 2 is a pair of complementary sequences, 800 nucleotides apart, that are predicted to form the stems of a strong double helix (18 bp, –32.3 kcal/mol). [score:11]
Figure 4. The ‘extended VCR’ of stratum 2 (shared by Homo and Pelodiscus sequences): (a) miR-16 target site (also shown in Fig. 2e) and nearby target sites for miR-376a, miR-335-3p, miR-493 and miR-379 (the Xenopus sequence contains a 44-bp insertion at the site of the asterisk that includes two target sites for miR-335-3p are shown in red); (b) conserved pair of target sites for miR-320a and miR-182; (c) conserved triplet of target sites for miR-378, miR-99a and miR-30aA notable feature of stratum 2 is a pair of complementary sequences, 800 nucleotides apart, that are predicted to form the stems of a strong double helix (18 bp, –32.3 kcal/mol). [score:11]
Either the miR-675 and miR-376 binding sites were targets for unidentified ancient microRNAs, perhaps still present in Pelodiscus and Callorhinchus, or the more recent imprinted microRNAs evolved to target sequences that were conserved for functions unrelated to binding by microRNAs. [score:5]
If the latter scenario is correct, then the VCR is likely to have been an original target of miR-675 and miR-376 which evolved to target its sequence. [score:5]
It is notable that miR-675 and miR-376 are both imprinted and maternally expressed [12, 27]. [score:3]
miR-376a, miR-379 and miR-493 are encoded in a large cluster of maternally expressed imprinted microRNAs found only in eutherian mammals [27]. [score:3]
This ‘extended VCR’ contains a remarkable concentration of predicted binding sites for microRNAs, including miR-335-3p [38], miR-376a [26] and miR-493 [39]. [score:1]
The miR-376 binding site occurs distal to the end of the short transcript. [score:1]
By contrast, miR-675 is known only from marsupial and eutherian mammals [35, 36] and miR-376 only from eutherian mammals [27]. [score:1]
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3
[+] score: 31
The combinatorial effect of ten down-regulated miRNAs (miR-144-3p, miR-33-5p, miR-32-5p, miR-1983, miR-136-5p, miR-142-3p, miR-376a-3p, miR-142-5p, miR-3968, and miR-29b-3p) reveals that a total of 61, 51, 48, and 37 target genes are significantly affected in PI3K-Akt, focal adhesion, cancer pathways, and transcriptional misregulation pathway respectively (p<0.001) (Figure 4). [score:7]
Two miRNAs miR-136-5p and miR-376a-3p down-regulated in SKH1 mice due to chronic UVR were also suppressed in wild type FVB mice skin due to UVR [13]. [score:6]
Ten miRNAs (miR-144-3p, miR-33-5p, miR-32-5p, miR-1983, miR-136-5p, miR-142-3p, miR-376a-3p, miR-142-5p, miR-3968, and miR-29b-3p) were differentially expressed (log fold change>1) and down-regulated in chronically treated SKH1 mice compared to untreated controls (Table 1-3). [score:5]
Figure 2 A-D. are showing the real time expression pattern of selected miRNAs miR-32-5p, miR-33-5p, miR-144-3p, and miR-376a-3p in untreated, acutely treated, and chronically treated SKH1 mice. [score:3]
All of these miRNAs (miR-32-5p, miR-33-5p, miR-144-3p, and miR-376a-3p) were down-regulated compared to their untreated littermates, and further confirms the findings of miRNA profiling study (Figure 2). [score:3]
Similarly, Mapk8 gene is targeted by three miRNAs miR-32-5p, miR-376a-5p, and miR-29b-3p. [score:3]
Figure 2Figure 2 A-D. are showing the real time expression pattern of selected miRNAs miR-32-5p, miR-33-5p, miR-144-3p, and miR-376a-3p in untreated, acutely treated, and chronically treated SKH1 mice. [score:3]
To confirm the findings of miRNA data, the validation pattern of miR-32-5p, miR-33-5p, miR-144-3p, and miR-376a-3p was analyzed in no UVR, acute, and chronic treated SKH1 skin samples. [score:1]
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4
[+] score: 25
Of a number of upregulated miRNAs, miRNA-376a, miR-127, miR-34a, miR-300, miR-342-3p were downregulated following metformin treatment in MCD-fed mice. [score:7]
The five downregulated miRNAs i. e., miRNA-376a, miRNA-127, miRNA-34a, miRNA-300 and miRNA-342-3p, were identical to five of the 71 upregulated miRNAs in control and MCD-fed mice. [score:7]
Notably, miR-122, miR-194, miRNA-101b, and miRNA-705 were upregulated and miRNA-376a, miRNA-127, miRNA-34a, miRNA-300 and miRNA-342-3p were downregulated in the liver tissue of MCD-fed mice treated with or without metformin (Table IB and Fig. 6). [score:7]
Recently, miR-376a downregulation has been shown to be associated with arsenic trioxide (ATO) -induced apoptosis in human retinoblastoma cells (16). [score:4]
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5
[+] score: 18
Normal miR-376a expression has been shown to be involved in the early fetal brain development, whereas accumulation of unedited miR-376a has been linked to neurodevelopmental disorders and increased metastasis potential of gliomas [83]– [86]. [score:5]
Down regulated mir-106b and up regulated miR-376a and miR-214 along with other modulated miRNAs at the acute stage of injury, may reflect the metabolic active state of neural tissue engaged in the immediate response to injury that involve neuroprotection, synaptic plasticity, axonal damage/regeneration, and neurogenesis. [score:3]
0112019.g007 Figure 7The fold upregulation of three miRNAs, miR-376a, miR-214 and miR-199a-3p, in the injury groups over the sham mice was validated using the individual real time PCR assays. [score:3]
The fold upregulation of three miRNAs, miR-376a, miR-214 and miR-199a-3p, in the injury groups over the sham mice was validated using the individual real time PCR assays. [score:3]
The expression profile of 3 out of 13 commonly modulated miRNAs, miR-199-3p, miR-214, and miR-376a that have been shown to be important in brain related processes and functions was also validated using the singleplex miRNA assay (Life Technologies, Carlsbad, CA) (Figure 7). [score:2]
Expression of miRNAs, miR-214, miR-376a and miR-199a-3p was validated using the singleplex miRNA assay (Life technologies, Carlsbad, CA; Assay# 002306, 001069 and 002304, respectively). [score:1]
MiR-376a was also up regulated in the serum of rats exposed to blast induced moderate TBI [22]. [score:1]
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6
[+] score: 14
Importantly, in the case of mir-376a-5p, mir-376b-5p, mir-376a-3p and mir-376-3p the edited nucleoside resides in the seed region, which is instrumental in targeting the miRNA to its target and could therefore lead to an altered target spectrum. [score:7]
The most abundantly edited miRNA is mir-376b, in the brain (Figure 2B), fitting with the observation that in murine and human brains, mir-376a/b/c are targets of the RNA editing machinery [51, 52]. [score:3]
Furthermore, we confirmed specific A to I editing in brain for mir-376a/b/c and identified mir-377 as a novel editing target. [score:3]
We find the mir-376a/c isoforms to be edited as well, albeit to a lesser extent (Figure 2B). [score:1]
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7
[+] score: 11
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-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-214, hsa-mir-200b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, 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-96, hsa-mir-200c, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-130b, hsa-mir-376a-1, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, hsa-mir-429, mmu-mir-429, hsa-mir-450a-1, mmu-mir-450a-1, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-130b, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, hsa-mir-450a-2, dre-let-7j, hsa-mir-376a-2, mmu-mir-450a-2, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
We found eight miRs differentially expressed, six down-regulated (miR-9, miR-141, miR-200a, miR-200b, miR-429 and miR-376a) and two up-regulated (miR-450a-5p and miR130b*) in the Dlx5 [−/−] OE (Fig.  1a). [score:9]
No Dlx5 binding site was predicted within a 50 kb range from the miR-9.1, miR-141, miR-200c and miR-376a loci. [score:1]
The miR-200a, - 200b and - 429 loci are closely located on chromosome 4, while miR-141 and -200c are closely located on chromosome 6. miR-376a is clustered with 16 other miRs on chromosome 12. [score:1]
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8
[+] score: 10
Editing in the seed sequence of miR-376 can also inhibit their targeting or lead to their retargeting to novel substrates (1, 16, 27). [score:7]
Editing in the seed sequence can lead to retargeting of the miRNA, which was already demonstrated for miR-376a-5p (former miR-376a*) (27). [score:3]
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9
[+] score: 10
miR-376a was induced between the 8-cell and morula stages, and rapidly downregulated upon blastocyst formation (Fig. 5c). [score:4]
We performed an equivalent analysis to identify miRNAs that are downregulated upon trophectoderm specification both in vitro and in vivo and identified one candidate miRNA, miR-376a (Fig. 5b). [score:4]
We investigated the expression of these nine candidate miRNAs (eight TE_up miRNAs in addition to miR-376a) in all preimplantation embryonic stages, ESCs, ES-TS cells, and BD-TS cells (Fig. 5c–d). [score:1]
miR-376a lies within a large imprinted cluster of miRNAs unique to placental mammals [57]. [score:1]
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10
[+] score: 8
F: qRT-PCR analysis was performed to assess the expression of miR-106a (i) and miR-376a (ii) in HCC cells treated with cisplatin. [score:3]
B and C: qRT-PCR analysis was performed to assess the expression of miR-376a and miR-122a in HCC cells treated with 5-fluorouracil (B) and pirarubicin (C). [score:3]
Importantly, miR-376a-P85α and miR-122a-Bcl-w[29- 30], which have been validated as deregulated axes in HCC cells, were modified after 5-fluorouracil and pirarubicin treatment, as shown by using qRT-PCR (Figure. [score:2]
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11
[+] score: 8
Preferential expression in the retina was also observed for miR-376a, miR-138, miR-338, and miR-136 as compared with the mouse platform; it is notable, however, that these miRs are expressed at higher levels in brain than in retina. [score:4]
Furthermore, the preferential expression in the retina of additional miRs, such as miR-376a and miR-691, represents a novel discovery. [score:3]
Additionally, novel retinal preference for miR-376a and miR-691 was identified. [score:1]
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12
[+] score: 8
We randomly picked 9 miRNAs (miR-337, miR-540-3p, miR-127, miR-434-5p, miR-329, miR-543-3p, miR-376a, miR-300, and miR-381) expressed from the Dlk1-Dio3 locus and validated their expression by qRT-PCR. [score:5]
108 ± 4.23, P = 0.091), whereas overexpression of the remaining 7 miRNAs (miR-127, miR-300, miR-329, miR-337-3p, miR-376a, miR-379, and miR-381) showed no significant effect on myotube diameter (Figure 2D). [score:3]
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13
[+] score: 7
The comparison between control- and MPA -treated cells revealed that 16 miRNAs were significantly modulated by more than two-fold (P < 0.05, Figure 1A), nine miRNAs were upregulated (miR-191*, miR-17*, miR- 470*, miR-451, miR-702, miR-434-3p, miR-493, miR-23a* and miR-485*) and seven were downregulated (miR-378*, miR-376a, miR-224, miR-190b, miR-16, miR-410 and miR-197) (Figure 1B). [score:7]
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14
[+] score: 7
Since possible target genes have been identified for only a few imprinted microRNAs, e. g. miR-134, miR-376a, miR-370, and the microRNAs embedded in the antisense transcript of the Retrotransposon-like 1 (Rtl1) gene [19, 22, 29- 32], we established a pipeline that combines different algorithms to predict microRNA target genes computationally. [score:5]
For example, the sequences with the highest overlap of 26.2%/48.8% (hsa-miR-376a and hsa-miR-376b) differ in only two bases (one in length and one base substitution). [score:1]
The murine sequence mmu-miR-376a is one nucleotide shorter and is aligned with two instead of three mismatches. [score:1]
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15
[+] score: 6
The canonical version of miR-376 and its seed-altered isomiR were shown to have highly distinct target sets [29], highlighting the biological importance of 5′-isomiRs. [score:3]
Perhaps the best-studied example of this phenomenon is the A-to-I editing of the miR-376 primary transcript leading to the expression of a 5′-isomiR of miR-376 with a modified seed [29]. [score:3]
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16
[+] score: 6
Importantly, the miRNAs miR-495-3p, miR-654-3p, miR-376a-3p and miR-487b-3p exhibited marked downregulation after 5 weeks in contrast to a slight reduction of expression observed for most miRNA genes from this region. [score:6]
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17
[+] score: 6
Wang et al. showed that following erythroid induction, miR-376a was significantly downregulated and CDK2 was released from miR-376a inhibition, thereby facilitating the escape of progenitor cells from the quiescent state into erythroid differentiation [43]. [score:6]
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18
[+] score: 6
The suppression of miR-155 was also discovered the study of the influence of several isoflavones from soy on prostate cancer cell lines, where miR-155, miR-208b, miR-211, miR-376a and miR-411 were found to be downregulated by the isoflavones by more than three to five fold than control cells [32]. [score:6]
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19
[+] score: 4
Importantly, the “transcriptional misregulation in cancer” pathway is affected by most of our differentially expressed miRNAs (miR-136-5p, miR-196a-5p, miR-196b-5p, miR-376a-3p, miR-335-5p, and miR-206-3p) significantly (p<0.001) (Figure 3A). [score:4]
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20
[+] score: 4
In the order of the significance score by SAM, 15 up-regulated miRNAs are mmu-miR-127, mmu-miR-410, mmu-miR-433, mmu-miR-138, mmu-miR-181c, mmu-miR-382, mmu-miR-19b, mmu-miR-381, mmu-miR-666-3p, mmu-miR-376a, mmu-miR-873, mmu-miR-181a, mmu-miR-383, mmu-miR-181b, and mmu-miR-99b. [score:4]
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21
[+] score: 4
Other miRNAs from this paper: hsa-mir-376a-1, hsa-mir-376a-2
Wang F., Yu J., Yang G. H., Wang X. S., Zhang J. W. Regulation of erythroid differentiation by miR-376a and its targets. [score:4]
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22
[+] score: 3
The miRNA OpenArray® screen also identified high expression of miR-376a in chondrocytes throughout the human developing limb. [score:3]
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23
[+] score: 3
Notably, microRNAs hsa-miR-127-5p, hsa-miR-370 and hsa-miR-376 had been shown to be highly and specifically expressed in islets of developing and adult human pancreas [53, 54]. [score:3]
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24
[+] score: 3
For example, Lee EJ 2007 et al. [44] showed that the miRNAs miR155, miR21, miR222, Let7, miR376a, miR301, miR100, miR125, miR142 and others are overexpressed significantly in human PC. [score:3]
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25
[+] score: 2
A similar situation can be found in the human cluster {hsa-mir-368, HP-37, HN-7, hsa-mir-376a} which corresponds to the mouse {mmu-mir-376a, mmu-mir-376b, MP-38}. [score:1]
The fine-grained structure of these loci has some species-specific aspects, as illustrated by Figures 2 and 3. The figures show all the validated miRNAs in these regions, including those with suboptimal prediction scores from the Additional files 7, 8, and 9. We find that some miRNAs that are related in sequence, and have presumably arisen by duplication (such as the mir-368/mir-376-related sequences) have different numbers of copies in rodents and human. [score:1]
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26
[+] score: 2
Again, miR-29b, miR-7a and miR-376a stimulated IFNa production in sera of treated mice, in contrast to miR-127 and miR-210. [score:1]
Three miRNA sequences, namely miR-29b, miR-7a, and miR-376a induced IL-12 secretion (Fig. 1A) and enhanced basal TNFa secretion (Fig. 1B), exceeding levels obtained for LPS and siRNA9.2 [21] positive controls. [score:1]
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27
[+] score: 2
So far, a number of non-coding regulators such as miR-451 (5, 6), miR-23a (7), miR-221/222 (8), miR-376a (9) and miR-223 (10) were reported to play positive or negative roles in controlling erythropoiesis. [score:2]
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28
[+] score: 1
Note that, for consistency, we refer to orthologous miRNAs according to how they are annotated in humans, for example, we use miR-376a-1 to denote both the human miRNA hsa-miR-376a-1 and the mouse miRNA mmu-miR-376a*. [score:1]
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29
[+] score: 1
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-21, hsa-mir-29a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-194-1, mmu-mir-200b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-140, hsa-mir-194-1, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-21a, mmu-mir-29a, mmu-mir-96, mmu-mir-34a, mmu-mir-135b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-376c, hsa-mir-376a-1, hsa-mir-135b, mmu-mir-181b-2, mmu-mir-376b, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-29a, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-140, dre-mir-181c, dre-mir-194a, dre-mir-194b, dre-mir-200b, dre-mir-200c, hsa-mir-376b, hsa-mir-181d, hsa-mir-507, dre-let-7j, dre-mir-135b, dre-mir-181a-2, hsa-mir-376a-2, mmu-mir-376c, dre-mir-34b, dre-mir-34c, mmu-mir-181d, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, mmu-mir-124b
Analysis of miR-376 RNA cluster members in the mouse inner ear. [score:1]
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[+] score: 1
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-16-1, hsa-mir-17, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-93, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-101a, mmu-mir-124-3, mmu-mir-125a, mmu-mir-130a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-136, mmu-mir-138-2, mmu-mir-140, mmu-mir-144, mmu-mir-145a, mmu-mir-146a, mmu-mir-149, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-185, mmu-mir-24-1, mmu-mir-191, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-204, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-204, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-138-2, hsa-mir-140, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-149, hsa-mir-185, hsa-mir-193a, hsa-mir-195, hsa-mir-320a, 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-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-93, mmu-mir-34a, mmu-mir-330, mmu-mir-339, mmu-mir-340, mmu-mir-135b, mmu-mir-101b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-107, mmu-mir-10a, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-320, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-29b-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-376a-1, hsa-mir-340, hsa-mir-330, hsa-mir-135b, hsa-mir-339, hsa-mir-335, mmu-mir-335, mmu-mir-181b-2, mmu-mir-376b, mmu-mir-434, mmu-mir-467a-1, hsa-mir-376b, hsa-mir-485, hsa-mir-146b, hsa-mir-193b, hsa-mir-181d, mmu-mir-485, mmu-mir-541, hsa-mir-376a-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, mmu-mir-301b, mmu-mir-674, mmu-mir-146b, mmu-mir-467b, mmu-mir-669c, mmu-mir-708, mmu-mir-676, mmu-mir-181d, mmu-mir-193b, mmu-mir-467c, mmu-mir-467d, hsa-mir-541, hsa-mir-708, hsa-mir-301b, mmu-mir-467e, mmu-mir-467f, mmu-mir-467g, mmu-mir-467h, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-467a-4, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, hsa-mir-320e, hsa-mir-676, mmu-mir-101c, mmu-mir-195b, mmu-mir-145b, mmu-let-7j, mmu-mir-130c, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
50E-0367mmu-miR-339-5pmir-3390.206.807.92E-037.53E-028mmu-miR-34c-5pmir-340.246.689.54E-066.88E-0477mmu-miR-34a-5pmir-340.179.541.17E-029.66E-0245mmu-miR-340-5pmir-3400.178.511.71E-032.45E-0217mmu-miR-361-5pmir-3610.247.887.74E-052.90E-0319mmu-miR-376b-3pmir-3680.268.451.05E-043.50E-0356mmu-miR-376a-3pmir-3680.1910.215.63E-036.40E-0223mmu-miR-434-3pmir-4340.2210.461.76E-044. [score:1]
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[+] score: 1
48) and miR-376a (ref. [score:1]
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[+] score: 1
Formosa A. Markert E. K. Lena A. M. Italiano D. Finazzi-Agro E. Levine A. J. Bernardini S. Garabadgiu A. V. Melino G. Candi E. MicroRNAs, miR-154, miR-299-5p, miR-376a, miR-376c, miR-377, miR-381, miR-487b, miR-485-3p, miR-495 and miR-654-3p, mapped to the 14q32. [score:1]
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