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miRBase |
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![]() 27 publications mentioning hsa-mir-519cOpen access articles that are associated with the species Homo sapiens and mention the gene name mir-519c. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary. |
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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-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, hsa-mir-10a, hsa-mir-34a, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-141, hsa-mir-146a, hsa-mir-155, hsa-mir-128-2, hsa-mir-34c, hsa-mir-20b, hsa-mir-431, hsa-mir-146b, hsa-mir-496, hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-548b, hsa-mir-663a, hsa-mir-663b, hsa-mir-1204, hsa-mir-1538, hsa-mir-103b-1, hsa-mir-103b-2
miR-519, a microRNA that suppresses tumorigenesis and lowers expression of RNA -binding protein HuR, was upregulated in senescent cells.
[score:8]
In conjunction with the finding that miR-519 reduced tumorigenesis in a xenograft mo del [32], we propose that the coordinated action of senescence -upregulated microRNAs can suppress tumor growth by reducing the levels of oncogenes or tumor promoters.
[score:6]
Among the microRNAs showing increasing abundance with senescence, miR-519 was of particular interest because it was shown to inhibit translation of HuR and to diminish tumor growth [31, 32].
[score:5]
miR-519 was recently found to inhibit translation of the RNA -binding protein HuR through its interaction with the HuR coding region [31].
[score:5]
As indicated above, miR-519 was found to suppress tumor growth [32].
[score:3]
Overexpression of miR-519 induced senescence in WI-38 and HeLa cells.
[score:3]
As shown here for miR-519, we postulate that these changes help to meet the needs of senescent cells in eliciting tumor suppression and growth arrest.
[score:3]
Since HuR potently enhances the expression of cancer-promoting proteins, and reducing HuR levels promotes HDF senescence [11, 38], we propose that miR-519 represses tumor growth at least in part, by lowering HuR and thereby promoting senescence (Figs. 4 and 5).
[score:3]
Additionally, miR-519 could further repress tumor growth by lowering the expression of other genes, such as ABCG2 or HIF-1α [46, 47].
[score:3]
In a separate study, miR-519 suppressed the growth of tumor xenografts in an HuR -dependent manner [32].
[score:3]
Accordingly, we postulate that one of the mechanisms by which miR-519 suppress tumor growth is by inducing senescence, and further propose that miR-519 triggers senescence -at least in part- by reducing HuR levels.
[score:3]
Given that HuR promotes cell proliferation and decreases senescence [33, 34], we hypothesized that the elevated miR-519 in senescent cells (Figure 4A) might lower HuR expression in WI-38 HDFs, and hence promote senescence.
[score:3]
We were particularly interested in the miR-519 family.
[score:1]
Together, these data indicate that miR-519 reduced HeLa cell proliferation and promoted HeLa cell senescence.
[score:1]
miR-519 -induced senescence in HDFs.
[score:1]
miR-519 -induced senescence in HeLa cells.
[score:1]
We previously reported that miR-519 represses the production of HuR, an RNA -binding protein which is highly abundant in cancer cells and is low in untransformed cells [11, 38].
[score:1]
Moreover, while HuR levels are high in tumors and low in normal tissues, miR-519 levels are high in normal tissues and low in cancer tissues [32].
[score:1]
Influence of miR-519 on the senescent phenotype of HeLa cells.
[score:1]
Influence of miR-519 on WI-38 senescence.
[score:1]
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Other miRNAs from this paper: hsa-mir-96, hsa-mir-302a, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-372, hsa-mir-373, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-498, hsa-mir-520e, hsa-mir-515-1, hsa-mir-519e, hsa-mir-520f, hsa-mir-515-2, hsa-mir-520a, hsa-mir-519b, hsa-mir-520b, hsa-mir-520c, hsa-mir-524, hsa-mir-519d, hsa-mir-520d, hsa-mir-520g, hsa-mir-517c, hsa-mir-520h, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-1323, hsa-mir-302e, hsa-mir-302f
However, construction of a Venn diagram showed that only 262 putative target genes are common between the miR-519 and miR-520 subfamilies in group I, indicating that the miR-519 and -520 subfamilies target different sets of genes.
[score:5]
Genes targeted by either or both the miR-519 or -520 subfamilies are shown in different color boxes.
[score:3]
Furthermore, one of the characteristics of target prediction, the sequence context surrounding the seed binding site of the target transcript [1], between the miR-519 and -520 subfamilies are also dissimilar (Fig. 2a).
[score:3]
The group I miR-519 subfamily also shares 262 putative target genes with the miR-302/-372 families, far fewer than the miR-520 subfamily (Fig. 3a, red box).
[score:3]
In this study, the putative target sets of the miR-519 and -520 subfamilies are overlapping gene sets predicted by two different prediction algorithms.
[score:3]
The group I miRNAs are composed of the miR-519 and -520 subfamilies.
[score:1]
Furthermore, it is noted that the AAGUGC seed position at 5’ end is variable among the C19MC-AAGUGC-miRNAs: subgroup I miRNAs, which includes eight miR-519 and -520 subfamilies, have the seed sequence located at the canonical and optimal 5’-nucleotide positions (nts) 2-7, as in the miR-302/-372 families; the seed sequence of the four subgroup IIa miRNAs is at location nts 1-6, and that of the remaining subgroup IIb miRNAs is at nts 3-8 and 4-9 (Fig. 2a).
[score:1]
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Other miRNAs from this paper: hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2
The mechanism underlying selective upregulation of the ORAI1 subunit is not known, but the post-transcriptional expression of the ORAI1 gene has been shown to be regulated by miR-519 using TargetScan/complementarity studies in HELA cells (Ab delmohsen et al., 2012).
[score:9]
Whether similar regulation by MIR-519 occurs in hVF-HF is not known, but in our studies we were unable to detect MIR-519 expression in fibroblasts from non-failing or failing hearts, which is suggestive that other possible regulatory mechanisms are involved (Sauc et al., 2015).
[score:5]
Growth inhibition by miR-519 via multiple p21-inducing pathways.
[score:3]
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Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-16-2, hsa-mir-192, hsa-mir-212, hsa-mir-215, hsa-mir-122, hsa-mir-191, hsa-mir-328, hsa-mir-423, hsa-mir-520h, hsa-mir-103b-1, hsa-mir-103b-2
We previously demonstrated that miR-328 levels negatively correlated with BCRP mRNA and protein expression levels in the human placenta 7. In addition, we reported that the expression levels of miR-328 were regulated by an epigenetic mechanism 7. The methylation patterns of several CpG dinucleotides proximal to two C/EBPα -binding sites in the miR-328 5′-flanking region negatively correlated with miR-328 levels, and positively correlated with BCRP protein levels in human placental samples 7. Other miRNAs such as miR-519c, miR-520h, and miR-212 also regulate the expression of BCRP 28 29.
[score:9]
Li et al. reported that miR-519c and miR-328 exerted stronger effects on the regulation of BCRP expression in human breast cancer cells than miR-520h 28.
[score:4]
Furthermore, epigenetic regulation may be involved in the expression of miR-519c and miR-520h.
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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-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-25, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-106a, hsa-mir-30c-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-143, hsa-mir-190a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-301a, hsa-mir-130b, hsa-mir-30e, hsa-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-369, hsa-mir-371a, hsa-mir-372, hsa-mir-373, hsa-mir-376a-1, hsa-mir-135b, hsa-mir-20b, hsa-mir-495, hsa-mir-181d, hsa-mir-520e, hsa-mir-515-1, hsa-mir-519e, hsa-mir-520f, hsa-mir-515-2, hsa-mir-520a, hsa-mir-526b, hsa-mir-519b, hsa-mir-525, hsa-mir-520b, hsa-mir-518b, hsa-mir-520c, hsa-mir-518c, hsa-mir-524, hsa-mir-517a, hsa-mir-521-2, hsa-mir-520d, hsa-mir-517b, hsa-mir-520g, hsa-mir-517c, hsa-mir-520h, hsa-mir-521-1, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-190b, hsa-mir-302e, hsa-mir-302f, hsa-mir-371b
In addition, we identified 12 other hES upregulated miRNAs in this cluster: miR-302a, miR-302b, miR-302c, miR-302d, miR-519b, miR-519c, miR-520a, miR-520b, miR-520c, miR-520d, miR-520e which share a consensus seed sequence: AAGUGC [24].
[score:4]
Among these miRNAs, miR-518b, miR-518c, miR-519b, miR-519c, miR-520a, miR-520c, miR-520e, miR-520g, and miR-524* are over-expressed in undifferentiated hES cells [24, 26, 29].
[score:3]
At the Gene Ontology level, miR-520b, miR-302b, miR-302c, miR-302d, miR-519c, miR-520a, and miR-302a formed a cluster (significant GO terms shown as red), and they shared GO terms related to chromatin structure modifications (Panel B).
[score:1]
MiR-520b, miR-302b, miR-302c, miR-302d, miR-519c, miR-520a and miR-302a were clustered closely base on the 48 GO terms analyzed.
[score:1]
In particular, miR-302a, miR-302b, miR-302c, miR-302d, miR-519b, miR-519c, miR-520a, miR-520b, miR-520c, miR-520d, and miR-520e had a consensus seed sequence: AAGUGC (Figure 8, panel A).
[score:1]
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Other miRNAs from this paper: hsa-let-7b, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-212, hsa-mir-222, hsa-mir-223, hsa-mir-15b, hsa-mir-137, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-184, hsa-mir-130b, hsa-mir-363, hsa-mir-371a, hsa-mir-372, hsa-mir-328, hsa-mir-339, hsa-mir-483, hsa-mir-146b, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-523, hsa-mir-518f, hsa-mir-520d, hsa-mir-518d, hsa-mir-548a-1, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-618, hsa-mir-625, hsa-mir-628, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-371b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az
Interestingly, we found miR-515-5p, miR-519c-3p, miR-520d-5p, miR-548a-3p, and miR-548c-3p specifically expressed in oocytes, and according to ExoCarta, these have not been found incorporated in exosome vesicles.
[score:3]
On the other hand, miR-515-5p, miR-519c-3p, miR-520d-5p miR-548a-3p, and miR-548c-3p, specifically expressed in oocyte, are not found incorporated in exosome vesicles.
[score:3]
Moreover, miR-515-5p, miR-519c-3p and miR-520d-5p, members of C19MC, which is a primate-specific cluster, seem to have a role in early embryo development during maternal-zygotic transition, when zygotic transcription starts and maternal mRNAs are degraded (Donker et al., 2012; Battaglia et al., 2016).
[score:2]
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Other miRNAs from this paper: hsa-mir-423, hsa-mir-520e, hsa-mir-519e, hsa-mir-520f, hsa-mir-520a, hsa-mir-519b, hsa-mir-520b, hsa-mir-520c, hsa-mir-519d, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-1324
Mir-519 and -519E were also upregulated in cKit+ ILCs; these microRNAs have been shown to inhibit cell growth and thus promote cell survival [25]whereas mir-423 promotes cell growth by regulating the G(1)/S transition in the cell cycle in hepatocellular carcinoma cell lines [26].
[score:7]
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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-100, hsa-mir-210, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-125b-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-1-1, hsa-mir-328, hsa-mir-433
Although two miRNAs, miR-328 and miR-519c, that have been previously described to downregulate human ABCG2 (Pan et al., 2009; To et al., 2009) have no fly orthologs, we report a reduction in miR-100, which is also predicted to bind to the human ABCG2 3′UTR (To et al., 2008).
[score:4]
Escape from hsa-miR-519c enables drug-resistant cells to maintain high expression of ABCG2.
[score:3]
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Many miRNAs that regulate the expression of HIF-1α directly or indirectly are detected, such as miR-210, miR-519c, miR-20a and miR-21 [3, 11, 15, 19, 28].
[score:6]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-16-1, hsa-mir-16-2, hsa-mir-181c, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-190a, hsa-mir-299, hsa-mir-30e, hsa-mir-302c, hsa-mir-373, hsa-mir-377, hsa-mir-328, hsa-mir-342, hsa-mir-135b, hsa-mir-376b, hsa-mir-520f, hsa-mir-520c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-527, hsa-mir-190b
Specifically, ABCG2 is downregulated by miR-519c in drug-sensitive cells via a binding site in the 3' UTR that is not present in their drug-resistant counterparts [62], and miR-520h targets ABCG2 in hematopoietic stem cells during their differentiation into progenitor cells [63].
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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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-210, hsa-mir-215, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-369, hsa-mir-371a, hsa-mir-340, hsa-mir-335, hsa-mir-133b, hsa-mir-146b, hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-499a, hsa-mir-504, hsa-mir-421, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-190b, hsa-mir-301b, hsa-mir-302e, hsa-mir-302f, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-371b, hsa-mir-499b
Small RNA regulation of some of the splicing control proteins has previously been reported; for example, the ELAV transcript, which encodes the HuR protein, a major modulator of mRNA stability and translation in addition to mRNA splicing [58], is subject to regulation by miRNAs miR-519, miR-16 and miR-125a in a variety of cell types including cervical, ovarian and colon cancer cell lines [59, 60, 61].
[score:5]
Ab delmohsen K. Srikantan S. Kuwano Y. Gorospe M. miR-519 reduces cell proliferation by lowering RNA -binding protein HuR levels Proc.
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Other miRNAs from this paper: hsa-mir-26a-1, hsa-mir-26b, hsa-mir-192, hsa-mir-147a, hsa-mir-34a, hsa-mir-122, hsa-mir-136, hsa-mir-186, hsa-mir-26a-2, hsa-mir-382, hsa-mir-452, hsa-mir-518c, hsa-mir-522, hsa-mir-601, hsa-mir-607, hsa-mir-608, hsa-mir-642a, hsa-mir-651, hsa-mir-320c-1, hsa-mir-891a, hsa-mir-147b, hsa-mir-548j, hsa-mir-1268a, hsa-mir-320c-2, hsa-mir-2052, hsa-mir-3162, hsa-mir-320e, hsa-mir-3191, hsa-mir-548x, hsa-mir-4313, hsa-mir-3614, hsa-mir-3617, hsa-mir-3620, hsa-mir-3665, hsa-mir-3681, hsa-mir-3912, hsa-mir-1268b
Following our initial analysis, overall, 11 differentially expressed miRNAs were identified, including miR-1268, miR-2052, miR-26b, miR-3665, miR-3681, miR-3912, miR-519c-3p, miR-601, miR-608, miR-720 and miR-891a.
[score:3]
Three miRNAs were up-regulated in Group B as compared to the other groups: miR-3665 (G), miR-519c-3p (H) and miR-891a (I).
[score:3]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-19a, hsa-mir-21, hsa-mir-22, hsa-mir-29a, hsa-mir-31, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, hsa-mir-148a, hsa-mir-210, hsa-mir-15b, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-126, hsa-mir-155, hsa-mir-29c, hsa-mir-373, hsa-mir-148b, hsa-mir-424, hsa-mir-429, hsa-mir-146b, hsa-mir-495, hsa-mir-520c
For example, mice injected with miR-107, miR-145, and miR-519c overexpressing tumor cells showed dramatically reduced HIF-1 levels, followed by suppressed tumor angiogenesis, growth, and metastasis [36– 38].
[score:5]
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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-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-29a, hsa-mir-16-2, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-200c, hsa-mir-331, hsa-mir-494, hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-548c
Recently identified miRNAs, such as miR-9, miR-34a, miR-16, miR-125a, miR-29a, miR-200c, and miR-519, play crucial roles in regulating HuR expression through interaction of miRNAs with specific sites in the 3′UTR and 5′UTR of the HuR mRNA.
[score:4]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-21, hsa-mir-25, hsa-mir-148a, hsa-mir-34a, hsa-mir-15b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-125b-2, hsa-mir-126, hsa-mir-378a, hsa-mir-148b, hsa-mir-451a, hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-589, hsa-mir-378d-2, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-378j
E) Quantification of SMYD2 protein level in HEK293T transfected with either pre-miR-519-3p or random miRNA sequences.
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D) Quantification of Smyd2 mRNA level in HEK293T transfected a plasmid containing either pre-miR-519-3p or random miRNA sequences.
[score:1]
F) Western-blot of HEK293T protein extract, transfected either with pre-miR-519-3p or random miRNA sequences.
[score:1]
Validation of Smyd2 mRNA interaction with miR-519.
[score:1]
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Other miRNAs from this paper: hsa-mir-378a, hsa-mir-378d-2, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-378j
The notion of escaping miRNA regulation via APA is also supported by additional examples, e. g. ABCG2 that escapes regulation by miR-519c by 3’UTR shortening in drug resistant cells [8], and Hsp70, which is alternatively polyadenylated upon ischemia or heat shock and thereby escapes miR-378* regulation [9].
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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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10b, hsa-mir-34a, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-215, hsa-mir-221, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-122, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-127, hsa-mir-194-1, hsa-mir-200c, hsa-mir-155, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-365a, hsa-mir-365b, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-135b, hsa-mir-424, hsa-mir-20b, hsa-mir-486-1, hsa-mir-491, hsa-mir-545, hsa-mir-590, hsa-mir-605, hsa-mir-663a, hsa-mir-663b, hsa-mir-1246, hsa-mir-302e, hsa-mir-302f, hsa-mir-203b, hsa-mir-486-2
[117] In contrast, miR-20b and miR-519c negatively regulate angiogenesis by targeting VEGF and/or HIF1α.
[score:4]
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18 |
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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-15a, hsa-mir-17, hsa-mir-19a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-10b, hsa-mir-34a, hsa-mir-182, hsa-mir-183, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-146a, hsa-mir-195, hsa-mir-155, hsa-mir-34b, hsa-mir-34c, hsa-mir-373, hsa-mir-146b, hsa-mir-519e, hsa-mir-519b, hsa-mir-520c, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-92b
MiR-519 represses the production of HuR, an RNA -binding protein very abundantly found in tumor cells and less expressed in untransformed cells, while the overexpression of HuR delays the senescent phenotype (83).
[score:4]
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19 |
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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-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-141, hsa-mir-200c, hsa-mir-29c, hsa-mir-200a, hsa-mir-302a, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-429, hsa-mir-520e, hsa-mir-520f, hsa-mir-520a, hsa-mir-519b, hsa-mir-520b, hsa-mir-518b, hsa-mir-520c, hsa-mir-518c, hsa-mir-520d, hsa-mir-520g, hsa-mir-520h, hsa-mir-302e, hsa-mir-302f
The miR-518b, miR-518c, miR-519b and miR-519c have been consistently reported to be overexpressed in undifferentiated hESCs [156, 166, 171, 172].
[score:3]
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20 |
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Other miRNAs from this paper: hsa-mir-198, hsa-mir-211, hsa-mir-144, hsa-mir-376c, hsa-mir-376a-1, hsa-mir-376b, hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-376a-2, hsa-mir-578, hsa-mir-548a-1, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-628, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-937, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az
For example, miR-144, miR-937, miR-376, miR-519, and miR-548A-3P are shown to regulate a number of mRNAs, and HCK, NFKBIE, IL6, SHMT2, and MCM4 are regulated by several miRNAs.
[score:3]
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21 |
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Other miRNAs from this paper: hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-34a, hsa-mir-203a, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-34c, hsa-mir-338, hsa-mir-449a, hsa-mir-495, hsa-mir-519b, hsa-mir-524, hsa-mir-520d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-561, hsa-mir-579, hsa-mir-590, hsa-mir-596, hsa-mir-607, hsa-mir-944, hsa-mir-548p, hsa-mir-664a, hsa-mir-203b, hsa-mir-664b
Following that, miR-19b, miR-19a, miR-520d-5p, miR-524-5p, miR-519b-5p, miR-519a, miR-519c-3p, miR-495, miR-944 and miR-664 regulate 121, 119, 130, 130, 109, 109, 109, 102, 138, 123 genes, respectively.
[score:2]
, miR-19b, miR-19a, miR-520d-5p, miR-519b-5p, miR-519a, miR-519c-3p, miR-944 and miR-664) are partially known (i. e., known to only human, but still unknown to rhesus).
[score:1]
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22 |
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Other miRNAs from this paper: hsa-let-7a-3, hsa-mir-15a, hsa-mir-16-1, hsa-mir-25, hsa-mir-28, hsa-mir-93, hsa-mir-16-2, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-15b, hsa-mir-9-1, hsa-mir-106b, hsa-mir-515-1, hsa-mir-519e, hsa-mir-515-2, hsa-mir-520a, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-579, hsa-mir-616
Our analysis shows a possible involvement of several members of the miR-515 family (such as miR-515-5p, miR-519 and miR-520a-3p/b/c-3p/d-3p/e/g/h), located at 19q13.4, in POF, since they are predicted to target FMR1 and FOXL2, two genes which are associated to POF [47], [48].
[score:3]
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23 |
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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-17, hsa-mir-30a, hsa-mir-100, mmu-let-7g, mmu-let-7i, mmu-mir-30a, mmu-mir-30b, mmu-mir-182, mmu-mir-187, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-182, hsa-mir-187, mmu-mir-290a, mmu-mir-294, mmu-mir-299a, mmu-mir-302a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-30b, 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-17, mmu-mir-100, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-299, hsa-mir-30e, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, hsa-mir-371a, hsa-mir-372, hsa-mir-373, mmu-mir-133b, hsa-mir-133b, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-520e, hsa-mir-515-1, hsa-mir-519e, hsa-mir-515-2, hsa-mir-520a, hsa-mir-519b, hsa-mir-520b, hsa-mir-517a, hsa-mir-519d, hsa-mir-521-2, hsa-mir-521-1, mmu-mir-367, hsa-mir-628, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, mmu-mir-743a, mmu-mir-743b, hsa-mir-888, hsa-mir-302e, hsa-mir-302f, hsa-mir-371b, mmu-mir-299b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-290b
Seed sequence examination indicated no similarities to the known seed sequences of pluripotency-specific miRNAs such as AAGUGC in miR-302b-3p, miR-373, miR-520e, miR-519c-3p, miR-520a-3p, and miR-520b; AGUGCC in miR-515-3p and miR-519e; and AAGUG in miR-519d.
[score:1]
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24 |
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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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-34a, hsa-mir-204, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-145, hsa-mir-188, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-381, hsa-mir-323a, hsa-mir-485, hsa-mir-517b, hsa-mir-449b, hsa-mir-657, hsa-mir-323b
47 (33) CDK6, DAPK1, PDGFRA, WEE1, MAP3K2, STK39, TRIB20.0214HSA-MIR-519C-5P.
[score:1]
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25 |
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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-21, hsa-mir-23a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-196a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-218-1, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-128-1, hsa-mir-145, hsa-mir-191, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-30c-1, hsa-mir-99b, hsa-mir-296, hsa-mir-30e, hsa-mir-361, hsa-mir-337, hsa-mir-148b, hsa-mir-196b, hsa-mir-425, hsa-mir-20b, hsa-mir-486-1, hsa-mir-488, hsa-mir-181d, hsa-mir-498, hsa-mir-520a, hsa-mir-526b, hsa-mir-520d, hsa-mir-506, hsa-mir-92b, hsa-mir-608, hsa-mir-617, hsa-mir-625, hsa-mir-641, hsa-mir-1264, hsa-mir-1271, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-30d, bta-mir-128-1, bta-mir-145, bta-mir-181a-2, bta-mir-30b, bta-mir-181b-2, bta-mir-20b, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-148b, bta-mir-181c, bta-mir-191, bta-mir-210, bta-mir-23a, bta-mir-361, bta-mir-425, bta-let-7g, bta-mir-30a, bta-let-7a-1, bta-let-7f-1, bta-mir-30c, bta-let-7i, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-99b, hsa-mir-890, hsa-mir-888, hsa-mir-889, hsa-mir-938, hsa-mir-1184-1, hsa-mir-1203, hsa-mir-1204, hsa-mir-1265, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-218-1, bta-mir-296, bta-mir-30f, bta-mir-486, bta-mir-488, bta-mir-92a-1, bta-mir-92b, bta-mir-1271, bta-mir-181a-1, bta-mir-181b-1, bta-mir-148c, hsa-mir-1184-2, hsa-mir-1184-3, hsa-mir-486-2, bta-mir-1264, bta-mir-148d
Among these, miR-938, miR-519c-3p, miR-1265, miR-498 and miR-488 were exclusively detected only in HE animals and 10 miRNAs including miR-608, miR-625*, miR-218-1*, miR-888*, miR-1184 and miR-1264 were detected only in SE and CE animal groups.
[score:1]
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Other miRNAs from this paper: hsa-mir-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-212, hsa-mir-221, hsa-mir-222, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-150, hsa-mir-195, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-335, hsa-mir-133b, hsa-mir-18b, hsa-mir-20b, hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-499a, hsa-mir-508, hsa-mir-208b, hsa-mir-499b
2010.00683. x 20649821 8. Ab delmohsen K. Srikantan S. Kuwano Y. Gorospe M. miR-519 reduces cell proliferation by lowering RNA -binding protein HuR levels Proc.
[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-93, hsa-mir-205, hsa-mir-211, hsa-mir-219a-1, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-125b-1, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-200c, hsa-mir-155, hsa-mir-219a-2, hsa-mir-331, hsa-mir-519e, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-659, hsa-mir-219b
The miR-659-3p cluster also included miR-219-3p and miR-519-5p (Fig. 1b), which had less significant or no association with PFS (p = 0.036 and p = 0.12, respectively).
[score:1]
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