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25 publications mentioning hsa-mir-513c

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-513c. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 138
Consistently, inhibiting MMSET expression using siRNA in Ishikawa cells transfected with miR-34a/miR-424/miR-513 inhibitor reduced the expression of Twist1 and Vimentin but elevated the expression of E-cadherin (Figure 5D). [score:11]
miR-34a, miR-424 and miR-513 directly target MMSET 3′-UTR to downregulate MMSET expression in EC cells. [score:9]
Consistently, our western blot data showed that transfection of miR-34a/miR-424/miR-513 reduced MMSET expression in HEC-1 cells, whereas transfection of miR-34a/miR-424/miR-513 inhibitor enhanced MMSET expression in Ishikawa cells (Figure 4D), suggesting that miR-34a/miR-424/miR-513 directly repress MMSET. [score:8]
Taken together, our data suggest that miR-34a/miR-424/miR-513 inhibits the invasive and stem cell-like properties of EC cells by suppressing MMSET expression via interacting with its 3′-UTR. [score:7]
We measured Twist1, Vimentin or E-cadherin mRNA by qPCR assay, and found that rescuing MMSET expression with MMSET ORF in the presence of miR-34a/miR-424/miR-513 mimic resulted in up-regulation of Twist1 and Vimentin and downregulation of E-cadherin (Figure 5C). [score:6]
The overexpression of MMSET ORF in HEC-1 cells partially rescued miR-34a/miR-424/miR-513 mimic -suppressed invasion and sphere formation (Figure 5A). [score:5]
Ectopic expression of miR-34a/miR-424/miR-513 in HEC-1 cells resulted in a significant decrease in the relative luciferase activity of MMSET 3′-UTR, but there was no inhibition of luciferase activity when the cells were transfected with miR-34a/miR-424/miR-513 mimic and mutant MMSET 3′-UTR (Figure 4C). [score:5]
To further validate the above observations, we investigated whether transient over -expression of a MMSET open reading frame (ORF) could reverse the inhibitory effects of miR-34a/miR-424/miR-513 mimic on EC cell invasion and sphere formation, or whether silencing of MMST with specific siRNA could repress the miR-34a/miR-424/miR-513 inhibitor -induced EC cell invasion and sphere formation. [score:5]
Our results demonstrated that the expression of miR-34a/miR-424/miR-513 is frequently lost in human EC tissues, and ectopic miR-34a/miR-424/miR-513 expression reduced EC cell sphere formation and invasion. [score:5]
In this study, we identified miR-34a/miR-424/miR-513 that could directly regulate MMSET expression in EC cells. [score:5]
For a set of 50 patients with EC, reduced expression of miR-34a/miR-424/miR-513 was significantly associated with a poorer prognosis of EC patients (Figure 6B), To explore whether the miR-34a/miR-424/miR-513-MMSET axis is clinically relevant, we assessed the correlation between the expression of miR-34a/miR-424/miR-513 and MMSET in EC tissues using qPCRs. [score:5]
EC cells (50% confluence) were transfected with miRNA mimics and miRNA inhibitors for miR-34a, miR-424 and miR-513 (40 nM, Ambion, Austin, TX), siRNAs against MMSET or Twist1 (5 nM, Ambion, Austin, TX) and the expression vector for MMSET (OriGene, Rockville, MD) using Lipofectamine 3000 (Invitrogen, Carlsbad, CA) according to the manufacturer’s instructions. [score:5]
Importantly, overexpression of miR-34a/miR-424/miR-513 inhibited invasion and sphere formation of HEC-1 cells (Figure 4E and 4F). [score:5]
Furthermore, in the present work, we provide new evidence that miR-513 can suppress EC cell sphere formation and invasiveness by targeting MMSET. [score:5]
miR-34a, miR-424 and miR-513 inhibit EMT, invasion and the sphere-forming ability of EC cells through targeting MMSET. [score:5]
We also found that repression of miR-34a/miR-424/miR-513 upregulates MMSET levels, thus promoting the invasion and sphere-forming ability of EC cells. [score:4]
Using qPCR analysis, we found that invasive HEC-1 cells had very low miR-34a/miR-424/miR-513 expression compared with less invasive Ishikawa cells (Figure 4B), indicating that the levels of miR-34a/miR-424/miR-513 were inversely correlated with MMSET expression in EC cells (Figure 1A). [score:4]
To determine if reduced miR-34a/miR-424/miR-513 expression is associated with any change in survival probability, we compared Kaplan-Meier plots for high and low expression of miR-34a/miR-424/miR-513. [score:4]
Moreover, the miR-34a/miR-424/miR-513 inhibitor -induced Ishikawa cell invasion and sphere formation were significantly reduced by MMSET siRNA (Figure 5B). [score:3]
However, Ishikawa cells transfected with miR-34a/miR-424/miR-513 inhibitor exhibited significantly increased cell invasion and sphere formation (Figure 4E and 4F). [score:3]
We detected a significant negative association between miR-34a/miR-424/miR-513 and MMSET mRNA expression (Figure 6C). [score:3]
We show that MMSET is a tumor promoter in EC, and the loss of miR-34a, miR-424 and miR-513 contributes to the overexpression of MMSET and aggressive phenotypes of EC cells. [score:3]
These observations suggest that miR-34a/miR-424/miR-513 are suppressors of EC cell invasion and sphere formation. [score:3]
To address the relevance of miR-34a/miR-424/miR-513 expression to human EC, we examined the levels of these miRNAs in primary ECs using qPCR analysis. [score:3]
In conclusion, our results demonstrate that MMSET exerts tumor-promoting effects in EC cells, and the loss of miR-34a, miR-424 and miR-513 enhances MMSET expression in EC. [score:3]
Figure 6(A) Relative miR-34a/miR-424/miR-513 expression in EC tissues and matched adjacent normal endometrial tissues. [score:3]
Mutation in the miR-34a, miR-424 or miR-513 -binding sequence was generated by using the QuickChange Mutagenesis Kit (Stratagene, La Jolla, CA). [score:2]
To test whether MMSET is directly regulated by miR-34a/miR-424/miR-513, we performed luciferase reporter assays by transfecting the reporter vector containing the full-length 3′-UTR of human MMSET into HEC-1 cells, together with miR-34a, miR-424, miR-513 or control mimic, respectively. [score:2]
Then, these predicted miRNAs were overlapped with a set of miRNAs that are significantly repressed in highly invasive EC cells [16], leading to the identification of 3 miRNAs (miR-34a, miR-424 and miR-513) (Figure 4A). [score:1]
Firefly luciferase reporter plasmid (100 ng) plus Renilla luciferase vector (10 ng), together with miR-34a/miR-424/miR-513 mimic or the negative control mimic, were transfected into HEC-1 cells using Lipofectamine 3000 (Invitrogen, Carlsbad, CA). [score:1]
miR-34a, miR-424 and miR-513 expression was measured using the NCode miRNA qRT-PCR analysis (Invitrogen, Carlsbad, CA) following manufacturer-recommended protocols. [score:1]
Figure 4(A) Alignment of miR-34a, miR-424 and miR-513 and their corresponding complementary binding sequences in MMSET 3′-UTR by bioinformatics algorithms. [score:1]
Figure 5(A) miR-34a/miR-424/miR-513 mimic or control mimic was co -transfected into HEC-1 cells, together with (or without) MMSET cDNA vector lacking the 3′-UTR region. [score:1]
Taken together, these results supported an existence of the miR-34a/miR-424/miR-513-MMSET axis in human EC. [score:1]
miR-34a/miR-424/miR-513 repression was associated with poorer prognosis of EC patients. [score:1]
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[+] score: 101
However, over the course of our study we observed significant up-regulation of both DR1 and BTG3 in the testis after sexual maturation of male rhesus macaques, and a negative correlation between the expression of DR1/BTG3 and miR-513, suggesting miR-513′s role on testicular development via its regulation of DR1 and BTG3. [score:8]
Notably, the miRNA -dependent inhibition of luciferase expression is specific for each member of the miR-513 subfamily (Figure  4), suggesting that different copies (miR-513a/b/c) with diverged seed sequences developed functional divergence by targeting different genes. [score:7]
To identify potential targets of miR-513 sequences, we used TargetScanS [15], and eight genes with top rank values were selected for functional testing. [score:5]
Previously, Zhang et al. reported that the miR-513 subfamily members are preferentially expressed in testis, and that expression decreases sharply during the course of sexual maturation in male rhesus macaques, suggesting that miR-513 may play some unknown functional roles in testis [6]. [score:5]
To further demonstrate whether miR-513b and miR-513c can inhibit the expression of DR1 and BTG3, we measured both mRNA and protein expression levels of endogenous DR1 and BTG3 in HeLa cells, after introducing the synthetic miR-513a/b/c and the negative control miRNAs. [score:5]
We found that miR-513b could significantly decrease the expression of DR1 both at the mRNA and protein levels, while miR-513c had no obvious impact on the mRNA and protein expression level of BTG3 (Figure  6). [score:5]
The results showed that miR-513a, miR-513b and miR-513c are all capable of targeting their predicted sites in the 3′UTRs of GNG13, DR1 and BTG3 respectively (Figure  4 and Additional file 1: Figure S5), while the remaining five genes showed no evidence of significant regulation (Additional file 1: Figure S6). [score:4]
Since the seed region of miRNA is critical for gene targeting, the between-copy nucleotide differences may potentially lead to functional divergence among gene copies of the miR-513 subfamily. [score:3]
Our observation suggests that miR-513b and miR-513c may affect the development of testis by regulating DR1 and BTG3. [score:3]
The Y-axis represents the ratio of Renilla luciferase (with candidate target gene’s 3′ UTR) activity to firefly luciferase activity after treated with negative control or miR-513 mimics. [score:3]
Our results showed that miR-513a, miR-513b and miR-513c are capable of specifically targeting their predicted sites in the 3′UTRs of GNG13, DR1 and BTG3 respectively. [score:3]
Luciferase analysis indicated that GNG13, DR1 and BTG3 are the respectively potential target genes of miR-513a, miR-513b and miR-513c. [score:3]
These observations collectively suggest that members of the miR-513 subfamily may play different roles in gene regulation. [score:2]
Interestingly, a significantly increased expression of DR1 and BTG3 in testis of adult macaques was observed as compared with the infant macaques measured by real-time quantitative PCR (Figure  5), which is negatively correlated with the expression of the miR-513 members [6]. [score:2]
Across primate species, there have been several duplication events and different species each possess a variety of miR-513 copies, indicating it underwent rapid evolution. [score:1]
Different copies of the miR-513 subfamily (miR-513a/b/c) have different seed sequences, due to after-duplication sequence divergences, which eventually led to functional divergences. [score:1]
Alignment of the miR-513 precursor sequences. [score:1]
For all three known great apes, there are two miR-513c copies in gorillas which were derived from miR-513b and lost in chimpanzees. [score:1]
Together, these results indicated that the miR-513 subfamily has a unique evolutionary history, quite different from other members in the same miRNA cluster. [score:1]
By contrast, the initial duplication event of the miR-513 subfamily seems to have occurred earlier in the common ancestor of Catarrhini. [score:1]
Functional divergence among gene copies of the miR-513 subfamily. [score:1]
MiR-513 is a rapidly evolving miRNA subfamily in primates. [score:1]
The ML tree of the miR-513 subfamily. [score:1]
Sequence comparisons showed that the duplicated copies of miR-513 were derived from transposable element (MER91C). [score:1]
Other genes of the miR-506-514 cluster, however, are not similar with MER91C, suggesting that the mechanism behind gene duplications in the miR-513 subfamily is different from the others. [score:1]
In the miR-506-514 cluster, the miR-513 subfamily has the greatest diversity in terms of both copy number and sequence variations [6]. [score:1]
Different copies of the miR-513 subfamily (miR-513a/b/c) with diverged seed sequences seem to have led to functional divergences. [score:1]
As reflected in the phylogenetic tree and sequence alignment of mature miR-513 sequences (Figure  2 and Additional file 1: Figure S4), miR-513b is probably the ancestral copy in Catarrhini, while miR-513a and miR-513c are derived copies generated by duplications. [score:1]
The miR-513 copies co-localized with MER91C and their sequence similarity. [score:1]
This inference was confirmed by the seed sequence comparison showing the same seed region in miR-513b with its orthologous copy in rats and an ancestral copy in the mouse lemur while both miR-513a and miR-513c have a single-base difference from miR-513b in the seed region (Additional file 1: Figure S4). [score:1]
In summary, we demonstrated that the miR-513 subfamily underwent multiple independent gene duplications among different lineages of primates. [score:1]
The chimeric gene tree of the miR-513 subfamily constructed by AnGST. [score:1]
All miR-513 copies are co-localized with MER91C and their sequences are similar (>50 identify; Additional file 1: Table S2). [score:1]
Instead, copies with same or similar mature miRNA sequences cluster together (Figure  2), indicating ancient duplications of miR-513 in the common ancestor of Catarrhini after the divergence from Platyrrhini (New World monkeys), but before the Old World species split. [score:1]
Sequence alignment suggests that miR-513c emerged independently in gibbons, and there are varied copies in great apes and humans (Figure  3). [score:1]
According to the miR-513 annotation in miRBase (http://www. [score:1]
By contrast, in Catarrhini (Old World monkeys, lesser apes, great apes and humans) the clustering of miR-513 copies is not in agreement with the accepted species phylogeny. [score:1]
Likewise, sequence divergences among the miR-513 copies have occurred, consistent with the previously proposed rapid evolution of the miR-506-514 cluster. [score:1]
Although there is no solid functional evidence, miR-513c emerged only in apes and humans, but shown sequence divergence in different lineages, implying that it may contribute to lineage-specific functions. [score:1]
MiR-513 is an X-linked miRNA subfamily with multiple copies that has undergone rapid evolution in primates. [score:1]
The after-duplication sequence divergences among the different copies of miR-513 led to functional divergence of these copies in primates. [score:1]
Gene copies of the miR-513 subfamily are named from “a” to “e” based on their sequences in miRBase. [score:1]
Sequence comparisons revealed that the duplicated copies of miR-513 were derived from transposable elements (MER91C), different from other members within the miR-506-514 cluster. [score:1]
Figure 2 Phylogenetic tree of the miR-513 subfamily. [score:1]
The miR-513 subfamily belongs to the miR-506-514 cluster located on the X chromosome. [score:1]
Figure 1 Distribution of the miR-513 subfamily in primates. [score:1]
Interestingly, most copies from the spider monkey cluster together, and the gene order of the eight miR-513 copies suggests a tandem duplication of a fragment containing three copies (e1-bL2-cL1/e2-bL3-cL2). [score:1]
Additionally, in Catarrhini, the formation of miR-513c was after the Old World species split and exists in apes and humans. [score:1]
Moreover, duplication events of the miR-513 subfamily seem to have occurred independently in Platyrrhini (New World monkeys) and Catarrhini (Old World monkeys, apes and humans) after they diverged. [score:1]
We analyzed the evolutionary pattern of gene duplications and their functional consequence for the miR-513 subfamily in primates. [score:1]
org) and remapping the miR-513 precursor sequences to primate species’ genomes that are sequenced (Additional file 1: Table S1), aside from one orthologous copy in the rat genome (rno-miR-3585), miR-513 exists only in primates. [score:1]
Interestingly, after alignment with known repeat sequences, the miR-513 copies seem likely to have been derived from MER91C (Additional file 1: Table S2), a DNA transposable element [7]. [score:1]
Notably, all miR-513aL/c copies have a single-base substitution (one of two sites) from their original sequence in gibbons and great apes, while the human miR-513c owns both substitutions (Figure  3). [score:1]
The miR-513 subfamily underwent multiple independent gene duplications among five different lineages of primates. [score:1]
Figure 3 Sequence alignment of mature miR-513c copies in gibbons, great apes and humans. [score:1]
More importantly, the after-duplication sequence divergences among the copies of miR-513 have led to functional divergence of these copies in primates. [score:1]
The miR-513 subfamily belongs to an X-linked primate-specific miR506-514 cluster. [score:1]
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[+] score: 44
0032999.g004 Figure 4(A) Expression of miR-513-3p, miR-571 and miR-652 was analyzed by qPCR in liver samples of patients with liver cirrhosis (n = 13) and livers from patients without chronic liver disease (n = 10) as control. [score:5]
Serum level of miR-513-3p, miR-571 and miR-652 were analyzed in a second collective of patients with chronic liver disease and patients without chronic liver disease (n = 13 each) in order to confirm that the alterations remain stable when patients instead of healthy individuals were used as control. [score:5]
0032999.g002 Figure 2(A) Serum levels of the three significantly regulated miRNAs (miR-513-3p; miR-571; miR-652) were analyzed by qPCR in a collective of 17 healthy controls and 67 patients with chronic liver disease and liver cirrhosis. [score:4]
Finally, ROC curve analysis showed that miR-513-3p, miR-571 and miR-652 were highly predictive for the presence of liver disease/cirrhosis (Figure 2 B). [score:3]
We next analyzed our array data with respect to miRNA regulations in serum between either different stages of liver cirrhosis or different etiologies in order to identify more specific stage- or etiology -dependent miRNAs, with a focus on the regulation of miR-652, miR-571 and miR-513-3p. [score:3]
Serum levels of miR-513-3p, miR-571 and miR-652 are significantly altered in the serum of patients with chronic liver disease and liver cirrhosis. [score:3]
Importantly, miR-652, miR-571 and miR-513-3p did not differ dependent on disease etiology (Figure 3 F). [score:3]
On one hand, increased levels of miRNAs such as miR-513-3p or miR-571 might reflect an epiphenomenon resulting from increased hepatic cell death in chronic liver disease, a hypothesis that cannot be ruled out on basis of our data. [score:3]
Next, we analyzed serum levels of miR-513-3p, miR-571 and miR-652 in a cohort of 17 healthy controls and 67 patients with chronic liver diseases by qPCR analysis (Table 1). [score:3]
Thus, the confirmation of our array results in a large cohort of liver disease patients by qPCR indicated an involvement of miR-513-3p, miR-571 and miR-652 in the pathogenesis of liver cirrhosis. [score:3]
Furthermore, to exclude a bias in regulation of these miRNA by co-morbidities or demographic differences, we correlated miR-652, miR-571 and miR-513-3p levels with age, gender, body mass index and serum creatinine concentration. [score:2]
In this larger collective, we observed a significant alteration for miR-513-3p, miR-571 and miR-652 in patients with liver cirrhosis, which was concordant to the previous findings in the array analysis (Figure 2 A). [score:1]
Interestingly, only levels of miR-571, but not of miR-652 or miR-513-3p, were concordantly regulated between serum and liver tissue from cirrhosis patients compared to healthy controls (Figure 4 A), suggesting that the liver is the primary source of serum miR-571 in cirrhosis patients. [score:1]
Figure S3 Confirmation of alterations of serum levels of miR-513-3p, miR-571 and miR-652 in a second cohort of patients. [score:1]
Furthermore, a hierarchical cluster analysis for miR-513-3p, miR-571 and miR-652 revealed two distinct subsets, one containing the control samples and the other containing all cirrhosis patients included into the array analysis (Figure 1 B), thus confirming the different abundance between patients and controls. [score:1]
In conclusion, using a systematic array approach on serum samples from patients with chronic liver disease, we identified etiology-independent alterations of serum levels of miR-513-3p, miR-571 and miR-652, three previously uncharacterized miRNAs. [score:1]
Of these three miRNAs, levels of miR-513-3p and miR-571 were significantly increased while levels of miR-652 were significantly decreased (Figure 1 A). [score:1]
However, only miR-513-3p, miR-571 and miR-652 reached statistical significance (Figure 1 B). [score:1]
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[+] score: 19
miRNA-513 was found to target the 3′ UTR of B7-H1, resulting in translational repression and ultimately leading to an inhibition of apoptosis when miR-513 was overexpressed (Gong et al. 2009). [score:9]
Overall, gene network analysis on putative targets for miR-494 and miR-513 lead us to speculate that these two miRNAs may play a role in the regulation of a cell’s inflammatory response. [score:4]
In response to the proinflammatory cytokine IFN-γ, miR-513 expression levels decrease and B7-H1 protein levels increase, subsequently leading to cell death (Gong et al. 2009). [score:3]
It has been shown recently that miR-513 plays a role in regulating interferon-γ (IFN-γ) -induced apoptosis. [score:2]
Although these studies were conducted in a different cell mo del from our study, these experimentally based findings support our computer-generated network analysis in that both types of analysis suggest that miR-513 family members may be participating in inflammatory signaling pathways. [score:1]
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[+] score: 15
Table S5 Compilation of target genes and/or genes co-regulated with hsa-miR-328, hsa-mir-494, hsa-mir-513 and hsa-mir-638. [score:4]
While lack of available experimental data precluded systematic questioning, we were able to analyze the target and/or co-regulated mRNAs for hsa-miR-328, hsa-miR-494, hsa-miR-513 and hsa-miR-638 (Table S5). [score:4]
Ten most significantly enriched processes for the genes targeted by hsa-miR-328, hsa-miR-494, hsa-miR-513 and hsa-miR-638 were scored and ranked in respect to the obtained p-values. [score:3]
Ontology enrichment analysis for target genes of hsa-miR-328, hsa-miR-494, hsa-miR-513 and hsa-miR-638. [score:3]
We found that all four mitomiRs were significantly involved in mitochondrial homeostasis, e. g hsa-mir-494 and hsa-mir-513 are both involved in ATP synthesis coupled electron transport (Figure 6). [score:1]
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[+] score: 13
Finally, miR-513 which targets the oncogene KRAS, the c-myc binding protein (MYCBP), MAPK7 which is a member of the mitogen-activated signal transduction pathway and the CD44 protein, which is a cell-surface glycoprotein involved in cell-cell interactions, cell adhesion and migration, was also down-regulated in our data set (Figure 3). [score:6]
At least eight miRNAs showed significant down-regulation between normal cervical samples and the pre-neoplasic and neoplasic samples, namely miR-143, miR-145, miR-99a, miR-26a, miR-203, miR-513, miR-29a and miR-199a. [score:4]
Eight miRNAs exhibited relative decreased expression with transition from normal cervix to atypical dysplasia to cancer (miR-26a, miR-143, miR-145, miR-99a, miR-203, miR-513, miR-29a, miR-199a) (Figure 4A). [score:3]
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[+] score: 9
Gong A. Y., Zhou R., Hu G., Li X., Splinter P. L., O'Hara S. P., LaRusso N. F., Soukup G. A., Dong H., and Chen X. M. (2009) MicroRNA-513 regulates B7-H1 translation and is involved in IFN-γ -induced B7-H1 expression in cholangiocytes. [score:5]
miR-513 is down-regulated in a STAT1 -dependent manner in IFN-γ -treated human biliary epithelial cells (30). [score:4]
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[+] score: 5
Other miRNAs from this paper: hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-513b
Gong AY Zhou R Hu G Li X Splinter PL O'Hara SP MicroRNA-513 regulates B7-H1 translation and is involved in IFN-gamma -induced B7-H1 expression in cholangiocytesJ Immunol. [score:5]
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[+] score: 5
In humans, miR-513 is located within a cluster (miR-506:514) that is overexpressed in melanoma [32]. [score:3]
In P. alecto, the novel miR-513 is also located within a putative cluster containing 14 other miRNAs (Figure  4b), the majority of which are novel. [score:1]
Four other miRNAs, representing homologs of miR-337, miR-377, miR-513c and miR-885 respectively, were also confirmed to have novel seed sequences in P. alecto. [score:1]
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[+] score: 4
miR-21 and miR-223 expression levels were increased in TGCTs, whereas the eight miRNAs in the miR-506~514 cluster (miR-506, miR-507, miR-508-5p, miR-510, miR-513a-5p, miR-513b, miR-513c and miR-514a-3p) were reduced in TGCTs as compared with NT. [score:2]
For mature miRNAs, cDNA was synthesized from 150 ng of total RNA and used to quantitate miR-506 (ID 001050), miR-510 (ID 002241), miR-514a-3p (ID 242955_mat), miR-513c (ID 002756), miR-513b (ID 002757), miR-513a-5p (ID 002090), miR-507 (ID 001051), miR-508-5p (ID 002092), miR-21 (ID 000397), miR-223 (ID 002295), miR-372 (ID 000560) and miR-373 (ID 000561). [score:1]
This cluster is conserved in primates, and consists of seven distinct miRNAs, that is, miR-506, miR-507, miR-508, miR-509, miR-510, miR-513 and miR-514. [score:1]
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[+] score: 4
Evidence shows that different members of the miR-513 subfamily (miR-513a/b/c) lead to functional divergences and that miR-513b can affect male sexual maturation by negatively regulating the development stage-related function of DR1 [9]. [score:3]
The miR-513 subfamily belongs to the miR-506–514 cluster. [score:1]
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[+] score: 4
A large number of overexpressed IR-responsive miRNAs that we identified in our work were found to be deregulated in human cancers, such as hsa-mir-513 [55], hsa-mir-744 [56], hsa-mir-92a [57], [58], hsa-mir-1228* [59], hsa-mir-671-5p [60], hsa-mir-638 [38], hsa-mir-370 [61], and hsa-mir-675 [62]. [score:4]
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[+] score: 4
Several mechanisms have been implicated in the regulation of PD-L1 expression by cancer cells such as activation of mitogenic and pro-survival pathways including MAPK and PI3K/AKT, increased activity of transcriptional factors HIF-1, STAT-3 and NF-κB, and presence of epigenetic modulators including miR-513, miR-570, miR-34a, miR-200 and miR-197 [14]. [score:4]
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[+] score: 3
34 hsa-miR-335 −0.35hsa-miR-345 [44], [53], [71] 1.16 hsa-miR-363 0.99 hsa-miR-371-5p 0.55 hsa-miR-421 0.50 hsa-miR-483-5p 1.33 hsa-miR-494 0.87 hsa-miR-505* −0.40 hsa-miR-513a-5p 1.06 hsa-miR-513b 1.19 hsa-miR-513c 1.22 hsa-miR-551b −0.40 hsa-miR-574-5p 0.97hsa-miR-630 [68], [73] 0.96 hsa-miR-769-5p −0.34 hsa-miR-801 0.66 hsa-miR-873 −0.64 hsa-miR-877* 0.72 hsa-miR-923 0.89 hsa-miR-940 0.49 hsa-miR-95 −0.44 hsa-miR-99a −0.64Irradiated and non-irradiated PBL of the same donors were incubated in static gravity (1 g) for 4 and 24 h, and miRNA expression profile was analyzed at the end of each incubation time. [score:3]
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[+] score: 2
2 complex hsa-miR-224-452 0.00168046 corum_3054 MAD1-mSin3A-HDAC2 complex hsa-miR-1912-1264 0.00316828 corum_3054 MAD1-mSin3A-HDAC2 complex hsa-miR-510-514 0.00316828 corum_422 Beta-dystroglycan-caveolin-3 complex hsa-miR-3671-101 0.00330472 corum_2436 ITGAV-ITGB1 complex hsa-miR-513c-513b 0.00333788 We next analyzed the spectrum of functions covered by our set of miRNA-regulated protein complexes. [score:2]
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Other miRNAs from this paper: hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, 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-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-98, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-199a-1, 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-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-222, hsa-mir-223, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-191, 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-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-195, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-363, hsa-mir-302c, hsa-mir-370, hsa-mir-373, hsa-mir-374a, hsa-mir-328, hsa-mir-342, hsa-mir-326, hsa-mir-135b, hsa-mir-338, hsa-mir-335, hsa-mir-345, hsa-mir-424, hsa-mir-20b, hsa-mir-146b, hsa-mir-520a, hsa-mir-518a-1, hsa-mir-518a-2, hsa-mir-500a, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-92b, hsa-mir-574, hsa-mir-614, hsa-mir-617, hsa-mir-630, hsa-mir-654, hsa-mir-374b, hsa-mir-301b, hsa-mir-1204, hsa-mir-513b, hsa-mir-500b, hsa-mir-374c
This study also uncovered a novel set of miRNAs like miR-222 and let-7f (associated with other malignancies), miR-513 and miR-223 (linked to immune regulation and related B-cell tumors), miR-424 (hematopoiesis), and miR-188 and miR-374 (no known physiological or pathological functions) [49]. [score:2]
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Another recent study found 7 abnormally expressed miRNAs (miR-145, miR-224, miR-150, miR-483-5p, miR-513-5p, miR-516a-5p, and miR-629) in SLE T cells compared to healthy controls. [score:2]
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), miR-513b and miR-513c. [score:1]
Fold induction could not be estimated for miR-513c in the microarray experiment: the signal was detectable upon induction, but was undetectable in uninduced control. [score:1]
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In addition, microRNAs, including miR-570, miR-513, miR-197, miR-34a, and miR-200, negatively regulate PD-L1 (100). [score:2]
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The importance of miRNAs in epithelial defense against pathogens was highlighted in biliary epithelial cells infected with the protozoan parasite Cryptosporidium parvum, an infection mo del in which let-7i and miR-513 contribute to the epithelial immune response. [score:1]
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As shown in Figure 3b (left panel) the Mann-Whitney test led to a pool of 11 miRNAs that were significantly associated to the immunoprecipitated HBsAg particles and were all contained within the group of HBsAg -associated human miRNAs identified by the comparative ΔΔC [T] analysis (Figure 3a) with the exception of miR-513-3p and miR-378 (Venn diagram in the Figure 3b, left panel). [score:1]
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Not surprisingly, only one miRNA (hsa-miR-513) was consistent with our differentially expressed miRNAs, suggesting that the biological characteristic of CCA is different from ICC. [score:1]
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This screen identified 10 microRNAs (miR-21, miR-19a, miR-17-5p, miR-26a, miR-26b, miR-107, miR-106b, miR-27a, miR-103, miR-25) that increased more than 50 % TFK-1 growth and 11 microRNAs (miR-513, miR-200b, miR-198, miR-200c, miR-520e, miR-429, miR-124a, miR-101, miR-29b, miR-494, miR-410) that decreased >50 % cell growth (Fig.   1c). [score:1]
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In human airway epithelial cells, diesel exhaust particles (DEP), the largest source of emitted airborne particulate matter (PM), induced miR-513b, miR-513c, miR-923, miR-494 and miR-338, and repressed miR-31*, miR-26b, miR-96, miR-27a, miR-135 and miR-374a. [score:1]
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MiR-let-7a, miR-7, miR-9, miR-513 and miR-220 families contain three or more copies distributed on the same or different chromosomes that produce identical or slightly differed mature miRNAs. [score:1]
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