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15 publications mentioning hsa-mir-510

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-510. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 281
Indeed, we show in vitro that overexpression of Akt1 leads to an increase in the expression of miR-510 and that inhibition of Akt1 results in a decrease in the expression levels of miR-510. [score:9]
To examine the role of Akt1 in the regulation of miR-510 expression we transfected MDA MB 175 VII cells, which express miR-510 at relatively high levels, with a short hairpin vector targeting Akt1 (shAkt1; Figure 2E, F). [score:8]
PRDX1 contains a miR-510 seed sequence in its 3'UTR and we have validated PRDX1 as a direct target of miR-510 and have shown how regulation of PRDX1 by miR-510 contributes to the migratory phenotype observed in miR-510 over -expressing cells. [score:7]
A PCR -based screen [21] was performed in order to identify novel targets of miR-510, as microRNAs are mainly thought to exert their effects through their negative regulation and direct binding to the 3'UTR of their target mRNA. [score:7]
In addition, we also see that Prdx1 protein and mRNA levels are increased in the miR-510 expressing cells when the Prdx1 ORF is transiently overexpressed (Figure 6A, B), suggesting that Prdx1 protein levels are restored to endogenous levels in the miR-510 expressing cells. [score:7]
Multiple targets of miR-510 are predicted to directly target multiple negative regulators and effectors of the Akt signaling pathway and, therefore, a potential mechanism of miR-510 -mediated increase in cell proliferation, migration, invasion and tumor growth could be through hyperactivation of the Akt signaling pathway. [score:7]
For the generation of clonal stable MCF10A cells overexpressing miR-510 (510-1; 510-10; 510-11), pSuppressor-neo vector (Imgenex, San Diego, CA, USA) expressing miR-510 was transfected into MCF10A cells and stable cells were selected in medium containing G418. [score:7]
We observed a small but significant decrease in migration when PRDX1 was overexpressed in scrambled control cells as well as a restoration of migration to control levels in miR-510 expressing cells when PRDX1 was co-expressed in both MCF10A and MCF7 cells (Figure 6C, D). [score:7]
We observed a decrease in the levels of Prdx1 protein in all of the cells tested when miR-510 was expressed, whereas the levels of Prdx1 mRNA were relatively unchanged, suggesting that miR-510 regulates Prdx1 through translational repression as opposed to mRNA degradation (Figure 5A, B). [score:6]
We show that miR-510 directly binds to the 3'UTR of PRDX1 and blocks its protein expression, thereby suppressing migration of human breast cancer cells. [score:6]
We have identified a novel role for PRDX1 in the inhibition of migration and demonstrate here that miR-510 mediated negative regulation of Prdx1 is able to inhibit both its role in migration as well as its more well-known role in cellular redox response. [score:6]
To test this hypothesis, we transiently overexpressed Akt1 in MCF10A cells and performed real time PCR to assess miR-510 expression levels (Figure 2D). [score:5]
miRNAs have multiple targets and, therefore, the effects observed after miR-510 expression may be the result of the increased Prdx1 protein, as well as non-Prdx1-related miR-510 effects. [score:5]
However, no further significant decrease in luciferase activity was observed in either the cells transfected with the PRDX mut construct or the EV control suggesting that miR-510 directly binds to the predicted site within the 3'UTR of PRDX1 to negatively regulate its expression. [score:5]
Based on our in vitro observations with the PI3K/Akt pathway and miR-510 expression, we performed IHC with p-Akt and observed an increased level of phosphorylated or active Akt in tumors expressing miR-510 (Figure 3C). [score:5]
Prdx1 expression inhibits miR-510 -mediated cell migration. [score:5]
To validate Prdx1 as a miR-510 target, and to examine whether Prdx1 expression is repressed by miR-510 through the predicted elements, a luciferase reporter construct containing the 3' UTR of Prdx1 was transfected into HEK293 cells (Figure 4E). [score:5]
However, by three weeks the miR-510 expressing tumors were growing more rapidly and by the end of the study, the miR-510 expressing tumors were larger (tumor volume) and heavier (tumor weight) than the scrambled controls (Figure 3A, B). [score:5]
They include its involvement in regulating expression of the serotonin receptor type 3 in enterocytes of colonic mucosa, indicating a role in irritable bowel syndrome [22, 23], as well as identifying elevated levels of miR-510 in Regulatory T cells (Tregs) from Type 1 diabetic patients [24]. [score:5]
To assess the functional effects of miR-510 when expressed at more physiological levels, we established stable breast cell lines expressing miR-510 after lentivirus transduction. [score:5]
Reciprocal to this we found that inhibition of miR-510 by transfection with either antisense oligonucleotides (ASO-510) or anti-miR510 vector (anti-510) in the breast cancer cell lines CAMA-1 (Figure 1G) and BT549 (Figure 1H) was able to inhibit migration in the presence of a stimuli as assessed by transwell migration assay. [score:4]
We observed an increase in luciferase activity in the cells treated with the PI3K inhibitor LY294002 when compared to the untreated control, suggesting that the PI3K/Akt pathway might be involved in the activation of miR-510 expression (data not shown). [score:4]
A greater comprehension of the mechanisms involved in miR-510 mediated tumor progression as well as the direct targets mediating these effects are critical to our understanding of its role in cancer. [score:4]
Peroxiredoxin 1 is a direct target of miR-510. [score:4]
These studies identify Peroxiredoxin 1 (PRDX1) as a novel direct target of miR-510. [score:4]
Click here for file Table 1. Direct targets of miR-510 identified in PCR screen. [score:4]
Peroxiredoxin 1 (Prdx1) is bioinformatically predicted and was identified through our screen to be a direct target of miR-510 (4A, Additional file 2, Table S1). [score:4]
Figure 5 miR-510 regulates endogenous PRDX1 protein expression. [score:4]
3'UTR: 3' untranslated region; ASO: antisense oligoribonucleotides; EGF: epidermal growth factor; EMT: epithelial-mesenchymal-transition; EV: empty vector; miR-510: microRNA 510; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; miRNA: microRNA; PI3K: phosphatidylinositide 3-kinase; PRDX1: peroxiredoxin 1; SRB: sulforhodamine B; Tregs: Regulatory T cells; UPL: universal probe library. [score:4]
To assess whether miR-510 was able to increase sensitivity to H [2]O [2 ]to similar levels as when PRDX1 is inhibited we performed cell viability assay with MDA MB 231 cells stably infected with miR-510 or scr control that were transiently transfected with a short hairpin functionally validated to target PRDX1. [score:4]
Transfection of antisense oligoribonucleotides (ASO) targeted against miR-510 (ASO-510) in CAMA-1 cells and anti-miR510 vector (anti-510) in BT549 cells resulted in an increase in Prdx1 protein levels, whereas the Prdx1 mRNA levels remained unchanged (Figure 5C, D). [score:3]
CAMA-1 and BT549 breast cancer cells were used as a mo del system to look at loss of function as they express miR-510 at the highest levels of all the breast lines examined. [score:3]
Our previous studies have shown that transient miR-510 expression increases the migration and invasion of non-invasive MCF7 breast cancer cells [15]. [score:3]
We also observed increased tumor growth when miR-510 was overexpressed in vivo. [score:3]
The study focused on peroxiredoxin 1 (PRDX1) as it was identified through our screen and was bioinformatically predicted to contain a miR-510 seed site in its 3' untranslated region (3'UTR). [score:3]
We show that miR-510 overexpression in non-transformed and breast cancer cells can increase their cell growth, migration, invasion and colony formation in vitro. [score:3]
To determine whether the PRDX1 3'UTR was responsive to miR-510 expression we transfected MDA MB 231 cells stably infected with miR-510 or scrambled controls with the luciferase reporter vectors (Figure 4F). [score:3]
Similarly cells overexpressing miR-510 showed an increased sensitivity to H [2]O [2], showing a 30 to 40% increase in cell death. [score:3]
Stable expression of miR-510 in MCF10A, MCF7 and MDA MB 231 cells was achieved through lentiviral infection. [score:3]
Colony formation was increased two- to six-fold in the mir-510 stably expressing clones. [score:3]
The reintroduction of PRDX1 into breast cancer cell lines without its regulatory 3'UTR confirmed that miR-510 was mediating its migratory phenotype at least in part through the negative regulation of PRDX1. [score:3]
Few targets have been identified for miR-510. [score:3]
To do this, the ORF of Prdx1 was transfected into the MCF10A and MCF7 miR-510 expressing cells and cellular migration assessed (Figure 6). [score:3]
Histologically, the tumors looked similar; however, Ki67 staining showed that the miR-510 expressing tumors were more proliferative than the scrambled controls (Figure 3C, D). [score:3]
Taken together, these data support a pivotal role for miR-510 in breast cancer progression and suggest it as a potential therapeutic target in breast cancer patients. [score:3]
Tumors from both miR-510 expressing and scrambled controls appeared to initiate at a similar time frame. [score:3]
We performed a PCR assay to identify novel direct targets of miR-510. [score:3]
To assess the effects of miR-510 on endogenous Prdx1 expression, both protein and RNA levels were assessed in MCF10A, MCF7 and MDA MB 231 cells. [score:3]
The cloning of miR-510 into pSuppressor-neo vector is already described [15]. [score:3]
Furthermore, we show in vivo that miR-510 expressing tumors have increased activation of the Akt pathway as demonstrated by an increase in Akt phosphorylation, suggesting that a positive feedback loop of this pathway may be occurring in these cells. [score:3]
As we have previously observed, the protein levels of Prdx1 were reduced in the miR-510 expressing cells (Figure 6A). [score:3]
However, the functional effects of miR-510 expression in non-transformed breast cells have not been assessed. [score:3]
Furthermore, the PI3K/Akt pathway was identified as a positive regulator of miR-510 both in vitro and in vivo. [score:2]
miR-510 expression was able to increase the ability of MCF10A cells (Figure 1D) and MCF7 cells (Figure 1E) to migrate in the absence of a stimuli as assessed by the Pacman haptokinetic migration track assay (Additional file 1, Figure S1). [score:2]
Figure 6 Functional effects of miR-510 mediated negative regulation of PRDX1. [score:2]
Lentiviral miR-510 and control vectors (pEZX) were purchased directly from GeneCopoeia (Rockville, MD, USA) and lentiviral preparations were made using the Maine Medical Center Research Institute cell culture and viral vector core (Scarborough, ME, USA). [score:2]
The goal of this study was to investigate the role of miR-510 in breast cancer cell migration and tumor growth and to verify PRDX1 as the direct miR-510 target underlying the mechanism of these phenotypic changes. [score:2]
We observed an increased repression of the PRDX1 3'UTR when miR-510 was expressed when compared to the scrambled controls. [score:2]
We performed real time PCR to assess miR-510 expression levels (Figure 2F) and observed a decrease in the levels of miR-510 in the shAkt1 transduced cells when compared to the scrambled control. [score:2]
The number of cells found to migrate or invade in miR-510 overexpressing cells was significantly increased compared with the parental control. [score:2]
Proliferation was assessed in breast cell lines that were stably infected with miR-510 over a course of seven days (Figure 2) and we observed a significant increase in the rate of cellular proliferation in MCF10A (Figure 2A), MCF7 (Figure 2B) and MDA MB 231 (Figure 2C) miR-510 expressing cells when compared to the scramble controls. [score:2]
Mutation of the seed sequence of miR-510 within the 3'UTR did not fully restore luciferase activity to the levels observed in the cells transfected with no 3'UTR construct, suggesting that other miRNA binding sites are present and functional within the 3'UTR of PRDX1. [score:2]
Prdx1 is an abundant antioxidant protein and we found that it was present in all cell lines examined (Figure 4B), but found no direct correlation between miR-510 and Prdx1 levels in the cell lines we examined (Figure 4B, D). [score:2]
We observed a significant (approximately seven-fold) increase in miR-510 levels in MCF10A cells overexpressing Akt1 compared to the empty vector control. [score:2]
Western blot of PRDX1 protein expression (A), quantitative real time PCR of peroxiredoxin 1 (PRDX1) mRNA levels (B) and quantified Pacman haptokinetic migration track assays (C) of miR-510 (510) or scrambled control (scr) MCF10A cells transiently transfected with PRDX1 ORF (PRDX1; light gray bars in B) or empty vector (EV; dark gray bars in B). [score:2]
However, no significant increase in sensitivity to H [2]O [2 ]was observed in cells with shPRDX1 and miR-510 expression when compared to either treatment alone. [score:2]
Breast cancer cell lines were transfected with pre-miR-510 or antisense miR-510 and western blotting and quantitative real time PCR were performed. [score:1]
qPCR of Akt1 (E) and miR-510 (F) levels in MDA-MB-175 VII breast cancer cells transduced with short hairpin Akt1 (shAkt) or scrambled control (scr). [score:1]
Exploring the role of miR-510 in metastasis may also allow it to be used as a biomarker and predictor of prognosis in patients, providing the next step toward personalized treatment in breast cancer. [score:1]
We performed Western blot (Figure 4B) and qPCR (Figure 4C, D) to assess the levels of endogenous PRDX1 and miR-510 levels in the various breast cell lines used in the study. [score:1]
Western blot (B) and quantitative PCR (C and D) analysis of endogenous PRDX1 (B and C) and miR-510 (D) levels in the cell lines used in the study. [score:1]
Our studies have shown that miRNA 510 (miR-510), is elevated in breast tumor samples while absent in the matched non-tumor breast tissue samples [15]. [score:1]
In this study, we provide evidence to support a role for miR-510 as a novel oncomir. [score:1]
Using three mir-510 independent clones we observe a two- to four-fold increase in migration (Figure 1A) and four- to five-fold increase in invasion (Figure 1B) across coated membranes. [score:1]
To assess the functional effects of miR-510 in vivo, we injected nude mice orthotopically with MDA MB 231 cells stably infected with miR-510 or scramble control as described above. [score:1]
Taken together these data suggest that the PI3K/Akt pathway may function in the activation of miR-510 in breast cancer. [score:1]
Transwell migration (A), matrigel invasion (B) and colony formation (C) assays of 3 independent stable clones over -expressing miR-510 (510-1, 510-10 and 510-11) compared to vector control (pSupp-4). [score:1]
GAPDH is shown as a loading control for western blot in B and is used for normalization in C and D. (E) Luciferase activity of HEK293 cells transfected with pGL3 promoter luciferase reporter vector alone (EV), the PRDX1 3'UTR reporter construct (PRDX 3'UTR) or PRDX1 3'UTR reporter construct mutated in the miR510 seed sequence binding site (PRDX mut). [score:1]
This study supports the role of miR-510 functioning as an "oncomir", causing increased migration, invasion and colony formation of non-transformed breast and non-invasive breast cancer cells in vitro and promoting breast tumor growth in vivo. [score:1]
Currently in the literature there are few studies highlighting the role of miR-510. [score:1]
Wild-type and miR-510 stably transformed MCF10A cells were seeded at a cell density of approximately 4 cells/mm [2 ]in normal growth media. [score:1]
To assess whether migration and/or invasion are altered in miR-510 overexpressing MCF10A cells, we performed transwell migration assays across a chemokine gradient, and invasion assays through Matrigel. [score:1]
The sequence complementary to the seed of miR-510 was deleted with the primers PRDX1mutF 5'-ttggtaggaatggcctggcgttgtgggcag-3' and PRDX1mutR 5'-ctgcccacaacgccaggccattcctaccaa-3' using a QuikChange Site-Directed Mutagenesis Kit (Stratagene, La Jolla, CA, USA). [score:1]
To further validate that the predicted miR-510 seed sequence within the PRDX1 3'UTR was functional, we mutated the seed sequence of miR-510 in the luciferase reporter construct. [score:1]
MicroRNA 510 promotes tumor growth in vivoTo assess the functional effects of miR-510 in vivo, we injected nude mice orthotopically with MDA MB 231 cells stably infected with miR-510 or scramble control as described above. [score:1]
A total of 1 × 10 [6 ]MDA-MB-231 cells stably transfected with either miR-510 or scramble control were injected orthotopically into eight-week-old female nude mice. [score:1]
We also observed the levels of miR-510 to be elevated in human breast tumor samples [15]. [score:1]
miR-510 affects the redox function of Prdx1. [score:1]
We have previously published the role of miR-510 in promoting migration, invasion and colony formation in breast cancer cells [15]. [score:1]
Panels show tumor volume (A), tumor weight (B), (C) and Ki67 quantitation (D) of tumors resulting from orthotopic injection of miR-510 (510) or scrambled control (scr) stably infected MDA MB 231 cells into female nude mice. [score:1]
To assess whether the miR-510 mediated negative regulation of PRDX1 was able to interfere with this primary function, we performed cell viability assay after treatment with H [2]O [2 ](Figure 6E, F). [score:1]
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[+] score: 41
Through qPCR, we found that the expression levels of these three miRNAs were all significantly down-regulated in mutant type (rs5951785 near hsa-miR-506, P=4.47×10 [−2], Figure 1A; rs5951785 near hsa-miR-507, P=4.80×10 [−3], Figure 2A; rs1447393 near hsa-miR-510, P=3.00×10 [−4], Figure 3A). [score:6]
The miR-510 expression level was significant down-regulated in mutant type compared with the wild type. [score:5]
Our results demonstrated that i) rs5951785 near hsa-miR-506/507 was associated with significantly increased risk of NOA, while rs1447393 near hsa-miR-510 decreased the risk of NOA; ii) rs5951785 significantly decreased binding affinity of hsa-miR-506, inhibited cell proliferation and promoted cell apoptosis. [score:3]
To understand the impacts of these two SNPs (rs5951785 near hsa-miR-506/507; rs1447393 near hsa-miR-510) on the miRNA expression, we transfer the wild-type pre-miRNAs and mutant pre-miRNAs into HEK-293T cells. [score:3]
PRDX1, a target gene of hsa-miR-510, was reported to participate in removing the ROS [22]. [score:3]
Besides, we also found hsa-miR-506 mutant-type significantly increased cell apoptosis (P=1.69×10 [−2], Figure 1D, 1E), while there was no difference in hsa-miR-507 nor hsa-miR-510 between the wild and mutant alleles (Figure 2D, 2E; Figure 3D, 3E), implicating that growth inhibition was accompanied with increased apoptosis population. [score:3]
Figure 3 A. RT-PCR was applied to detected mature miR-510 expression levels. [score:3]
A. RT-PCR was applied to detected mature miR-510 expression levels. [score:3]
C. CCK8 was used to determine the influence of rs1447393 near miR-510 on cell growth. [score:1]
Eventually, two SNPs (rs5951785 and rs1447393), located near the regions of hsa-miR-506/507 and hsa-miR-510, were found to be associated with NOA, and in vitro analysis was performed to clarify their potential functions in spermatogenesis. [score:1]
The cell growth was markedly increased at 48h (P=4.16×10 [−2]) and 72h (P=4.90×10 [−3]) with hsa-miR-510 mutant allele (Figure 3C), indicating that rs1447393 near hsa-miR-510 promoted cell proliferation. [score:1]
There was no difference of cell cycle between miR-510 wild and miR-510 mutant type. [score:1]
It was significantly increased in miR-510 mutant type for PRDX1. [score:1]
The cell growth was markedly increased with miR-510 mutant type at 48h. [score:1]
Through conducting dual-luciferase reporter assay, we found that the luciferase activities of CDK4, GLI3, PIK3C2A, ADAM17, SFRP2 and PRDX1 were significantly decreased when compared to the vectors, suggesting that they were the potential targets of hsa-miR-506, hsa-miR-507 and hsa-miR-510, respectively (Figure 1B, 2B, 3B). [score:1]
F, G. Effects of rs1447393 near miR-510 on cell cycle were determined by flow cytometry. [score:1]
Functional analysis indicated that rs1447393 near miR-510 might protect from the risk of NOA. [score:1]
Only rs547043 near hsa-miR-4330, rs5951785 near hsa-mir-506/507, rs1447393 near hsa-mir-510, and rs5985440 near hsa-miR-652 were retained associated with NOA, among which rs547043 near hsa-miR-4330 was inconsistent with screening stage. [score:1]
In conclusion, rs5951785 near hsa-miR-506/507 and rs1447393 near hsa-miR-510 were identified to be potential modifier of NOA. [score:1]
There was no significant difference of cell apoptosis in rs1447393 near miR-510. [score:1]
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[+] score: 15
Recently, Hezova et al. [24] demonstrated that miR-510 expression was elevated in regulatory T cells of diabetic patients. [score:4]
MiR-510 and miR-659 were over-expressed under diabetic-like conditions and decreased after calcitriol was added. [score:3]
MiR-510 was first identified in association with irritable bowel syndrome; its co -expression was involved in the regulation of 5-HT [3] receptors in colonic enterocytes [23]. [score:3]
To the best of our knowledge, our findings are the first demonstration of miR-510 involvement in HUVEC exposed to a diabetic-like environment with significant changes induced by calcitriol. [score:1]
In addition, 10 [-10] mol/l calcitriol was given to the cells 1 h after stimulation for an additional 23 h. The miRNA set that included (A) miR-659, (B) miR-510, (C) miR-181C, (D) miR-411, (E) miR-126, (F) miR-15a, and (G) miR-20b was validated using real time PCR. [score:1]
From the miRNA list presented in Table  1 and from the corresponding Venn diagram (Figure  1C), we validated several miRNA (marked in bold in Table  1) that are known to be modified in a diabetic environment (miR-510, miR-15a, miR-20b, miR-126, and miR-181C). [score:1]
MiR-181c, miR-15a, miR-20b, miR-411, miR-659, miR-126 and miR-510 were selected for further analysis because they are known to be modified in DM and in other biological disorders. [score:1]
Manipulation of miR-510 may represent a beneficial effect of calcitriol if we consider the possible deleterious effect of increased miR-510 in DM. [score:1]
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[+] score: 12
WST-1 colorimetric assay (11644807001; Roche Diagnostics, Indianapolis, IN, USA) was performed to determine the effects on cell viability from overexpression of miR-510 or miR-514a-3p. [score:2]
Using the, we showed that overexpression of miR-510 or miR-514a-3p in TCam-2 cells reduced cell viability (15% and 24%, respectively; P<0.05) as compared with the NC -treated cells (Figure 2a). [score:2]
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]
Overexpression of miR-510 or miR-514a-3p also induced apoptosis (13% and 17%, respectively), as demonstrated by the caspase-3 activity assay (Figure 2b). [score:2]
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]
Functional studies of miR-510 and miR-514a-3p in TGCT cell lines. [score:1]
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]
For miRNA mimics, cells were transfected with three different concentrations (5, 25 and 50 nM) of mirVana miR-510 mimic (MC12923), miR-514a-3p mimic (MC13114) or miRNA mimic Negative Control #1 (NC, ID_4464058) using siPORT NeoFX transfection agent (Life Technologies). [score:1]
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[+] score: 9
The miRNAs that exhibited at least a 2-fold change in expression in the hADSCs before and after the induction of chondrogenic differentiation are listed in Table I, and these include 12 upregulated miRNAs (miR-196a, miR-143, miR-383, miR-193b, let-7i, miR-26a, miR-539, miR-199a-3p, miR-337-5p, miR-146a-5p, miR-646, and miR-381) and 8 downregulated miRNAs (miR-490-5p, miR-1307, miR-125b, miR-96-3p, miR-302-3p, miR-23a-3p, miR-590, and miR-510). [score:9]
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[+] score: 4
Functional validation showed that the variant results in increased expression of pre-miR-510, miR-510-5p, and miR-510-3p (Feng et al., 2009; Sun et al., 2009). [score:3]
An example of a pri-miRNA variant affecting the first processing step is a variant located four bases upstream of the miR-510-5p sequence. [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-641
Computer simulation [32] suggests that the 3′UTR SNPs rs3746544 and rs1051312 (map within the associated region of this study) may alter the binding site of microRNAs (miR-510- miR-641) and consequently influence the level of SNAP-25 expression. [score:3]
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[+] score: 3
Specifically we can map hsa-miR-122, hsa-miR-495, hsa-miR-34b, hsa-miR-198, hsa-miR -202, hsa-miR-510 and hsa-miR-658 to expression derived from diverse tissues of origin (Table S3), supporting the hypothesis that non-hematopoietically derived miRNAs can enter and persist in circulation. [score:3]
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[+] score: 3
Kapeller J. Houghton L. A. Monnikes H. Walstab J. Moller D. Bonisch H. Burwinkel B. Autschbach F. Funke B. Lasitschka F. First evidence for an association of a functional variant in the microRNA-510 target site of the serotonin receptor-type 3E gene with diarrhea predominant irritable bowel syndromeHum. [score:3]
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[+] score: 3
Thus far, the 10 miRNAs, that is, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, and hsa-miR-6865-5p, do not have any known function in human and other animals. [score:1]
Other hairpins MD5, MD17, MD157, MD244, MD366, MR175, MR201, MR268, and MR282 were aligned with hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, and hsa-miR-342-3p, respectively. [score:1]
The utility of those 13 miRNAs, that is, hsa-miR-628-5p, hsa-miR-6804-3p, hsa-miR-4289, hsa-miR-208a-3p, hsa-miR-510-3p, hsa-miR-18a-3p, hsa-miR-329-3p, hsa-miR-548ax, hsa-miR-3934-5p, hsa-miR-4474-5p, hsa-miR-7974, hsa-miR-6865-5p, and hsa-miR-342-3p, can be utilized as antiviral therapeutics against MERS-CoV infection. [score:1]
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[+] score: 2
yes from Czech republic[68] diarrhoea predominant irritable bowel syndrome miR-510 HTR3E rs56109847 (previously rs62625044) G>A (A impairs binding site) in vitro: reporter gene assay in HEK293 and Colo320 cells (with miR precursor, miR inhibitor or negative control). [score:2]
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[+] score: 2
P1-LC) 8-mer 4th hsa-miR-510 HTR3E 18614545 rs3731563 3: 48199695 T C. [score:1]
P1) 7-8mer 8th hsa-miR-206 ESR1 17312270 rs11551509 6: 34505633 C A NA 8-mer 8th hsa-miR-510 SPDEF 18922924 rs8829 7: 148504618 A C 1 (CEPH) 8-mer 2nd hsa-miR-101 EZH2 20478051 rs78899540 7: 27181092 A C. [score:1]
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[+] score: 2
Hsa-mir-510, -152 and -484 which occur predominantly in Alu insertions are enriched in the category ‘transcription regulation’; hsa-mir-128b, -378 and -452 – in ‘cell cycle’. [score:2]
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[+] score: 1
A miRNA microarray analysis recently identified that miR-509 members and miR-510, which were not included in the microRNA PCR plate used in this study, could clearly distinguish OCCC from HGSC [22]. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-508
Additionally, Zhang et al. [17] have reported that three human X-linked testis miRNAs, miR-513-1, miR-508 and miR-510, have an excess of substitutions over neutrality and are under positive selection. [score:1]
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