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50 publications mentioning hsa-mir-495

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-495. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 293
However, the miR-495 inhibitor could further increase the high glucose -induced upregulation of MMP-2, MMP-9, collagen I and collagen III expressions and downregulation of TIMP-1 expression (Fig. 4a, b). [score:13]
Overexpression of miR-495 attenuated high glucose -induced CF inflammation and differentiation into myofibroblasts, downregulated MMP expressions, and reduced collagen production through inhibition of the NF-κB and TGF-β1/Smad signaling pathways by directly targeting NOD1. [score:13]
Our results also showed that overexpression of miR-495 significantly inhibits the high glucose -induced NF-κB and TGF-β1/Smad signaling pathways by downregulating NOD1 expression. [score:10]
Upregulation of miR-495 ameliorates the high glucose -induced inflammatory, cell differentiation and extracellular matrix accumulation of human CFs by modulating both the NF-κB and TGF-β1/Smad signaling pathways through downregulation of NOD1 expression. [score:9]
Moreover, the high glucose -induced NOD1 expression in CFs was downregulated by miR-495 overexpression. [score:8]
Moreover, TIMP-1 expression in the supernatants of CFs was downregulated after high glucose treatment, while the miR-495 mimic blocked the high glucose -induced reduction in TIMP-1 expression (Fig. 4a). [score:8]
Upregulation of miR-495 evidently inhibited the increase in high glucose -induced α-SMA expression at the mRNA and protein levels (Fig. 3a). [score:8]
In line with the altered MMP expressions, the mRNA expressions of collagen I and III were significantly higher in the high glucose group, whereas introduction of miR-495 inhibited the effect of high glucose (Fig. 4b). [score:7]
These results confirm that upregulation of miR-495 can protect CFs from high glucose -induced cardiac fibrosis through the modulation of the NF-κB and TGF-β signaling pathways by directly targeting NOD1. [score:7]
The miR-495 inhibitor, miR-495 mimic, miR -negative control for the inhibitor (miR-NC inhibitor), miR -negative control for the mimic (miR-NC) were synthesized and purified by RiboBio. [score:7]
Overexpression of miR-495 inhibited WT NOD1 reporter activity but not the activity of the mutated reporter construct in human CFs, showing that miR-495 could specifically target the NOD1 3’UTR by binding to the seed sequence (Fig. 5b). [score:7]
control or normal glucoseSubsequently, the online database (TargetScan 6.2) predicted several miRNAs that could directly target NOD1, including miR-605, miR-924, miR-3194-3p, miR-495 and miR-4477a. [score:6]
Importantly, miR-495 overexpression could significantly inactivate the high glucose -induced NF-κB and TGF-β signaling pathways by downregulating the levels of p-IKK/t-IKK, p-IκBα/t-IκBα, p-NF-κB/t-NF-κB and p-Smad3/t-Smad3. [score:6]
Our results show that the introduction of miR-495 ameliorates high glucose -induced inflammatory reactions, cell differentiation and extracellular matrix accumulation of human CFs via the modulation of the NF-κB and TGF-β1/Smad signaling pathways by downregulation of NOD1 expression. [score:6]
Furthermore, high glucose -induced upregulation of NOS2 and COX2 were significantly further increased in CFs transfected with miR-495 inhibitor (Fig. 2a, b). [score:6]
control or normal glucose Subsequently, the online database (TargetScan 6.2) predicted several miRNAs that could directly target NOD1, including miR-605, miR-924, miR-3194-3p, miR-495 and miR-4477a. [score:6]
Furthermore, miR-495 downregulation promoted high glucose-stimulated expressions of α-SMA (Fig. 3b). [score:6]
Introduction of miR-495 significantly decreased the expression of NOD1, whereas knockdown of miR-495 increased the NOD1 expression in CFs (Fig. 5c). [score:6]
As expected, high glucose -induced upregulation of NOS2 and COX2 was markedly attenuated in human CFs overexpressing miR-495 (Fig.   2a, b). [score:6]
CFs were transfected with miR-495 inhibitor or mimic for 48 h, and then treated with 5.5 or 25 mM glucose for 24 h. HG + miR-NC indicates CFs transfected with the miR-495 inhibitor before treatment with high glucose; HG + miR-495 mimic indicates CFs transfected with the miR-495 mimic before treatment with high glucose. [score:5]
These data indicate that miR-495 directly regulates NOD1 expression through 3’UTR sequence binding. [score:5]
Our results show that the expressions of TGF-β1, p-Smad3 and PAI-1 were significantly higher after treatment with high glucose, whereas overexpression of miR-495 could effectively block the effect of high glucose (Fig. 6a, b). [score:5]
In our study, we demonstrated that MMP-2 and MMP-9 levels in CFs increased significantly in response to high glucose, and that was reversed by overexpression of miR-495 and further increased by inhibition of miR-495. [score:5]
We found that high glucose promoted collagen I and III synthesis in CFs, and that this was partially inhibited by overexpression of miR-495. [score:5]
The miR-495 inhibitor (100 nM), mimic (50 nM), miR-NC inhibitor (100 nM) and miR-NC (50 nM) were transfected into CFs using Lipofectamine 3000 reagent (Invitrogen) according to the manufacturer’s protocols. [score:5]
Fig. 1The expressions of NOD1 and miR-495 in human CFs incubated with normal (5.5 mM) or high (25 mM) glucose for 6, 12, 24 or 48 h. a The mRNA expression of NOD1 was detected via quantitative RT-PCR. [score:5]
Also, the expressions of COX2, NOS2, TGF-β1 and PAI-1 induced by high glucose were markedly reduced after overexpression of miR-495. [score:5]
Human CFs were transfected with miR-495 inhibitor or mimic for 48 h. a Schematic representation of NOD1 3’UTRs showing putative miRNA target site. [score:5]
miR-495 can directly target NOD1 in HCFs. [score:4]
To validate whether NOD1 is a direct target of miR-495, luciferase plasmids containing the potential NOD1 miR-495 -binding sites (WT) or a mutated NOD1 3’UTR were constructed (Fig. 5a). [score:4]
We found that NOD1 is a direct target of miR-495 in CFs. [score:4]
Upregulation of miR-495 significantly alleviated the high glucose -induced increases in cell differentiation and collagen accumulation of CFs. [score:4]
Fig. 5NOD1 was a direct target of miR-495. [score:4]
The expression of NOD1 was significantly higher and the level of miR-495 was significantly lower in human CFs incubated with high glucose. [score:3]
The vehicle is transfection reagent alone To gain further insights into the potential roles of miR-495 in cardiac fibrosis, we determined the MMP expressions and collagen synthesis in the supernatants of CFs. [score:3]
The luciferase reporter assay showed that miR-495 can directly target NOD1. [score:3]
These findings provide further evidence for the protective effect of miR-495 overexpression on high glucose -induced cardiac fibrosis. [score:3]
The vehicle is transfection reagent alone The online database TargetScan 6.2 was used to identify an miR-495 -binding site in the 3’UTR of NOD1 (Fig.   5a). [score:3]
These results provide further evidence for the protective effect of miR-495 overexpression in cases of high glucose -induced cardiac fibrosis. [score:3]
The vehicle is transfection reagent alone To explore the effect of miR-495 on the differentiation of human CFs into myofibroblasts in vitro, we treated human CFs with high glucose for 24 h after transfection with the miR-495 mimic or inhibitor. [score:3]
Human CFs were transfected with an miR-495 inhibitor or mimic and incubated with high glucose. [score:3]
The data also indicate that overexpression of miR-495 attenuated differentiation of CFs into myofibroblasts. [score:3]
These findings indicate that miR-495 overexpression prevents high glucose -induced differentiation of CFs. [score:3]
Our data show that introducing miR-495 obviously decreased the high glucose -induced expressions of p-IKK/t-IKK, p-IκBα/t-IκBα and p-NF-κB/t-NF-κB (Fig.   6a). [score:3]
In this study, we showed that high glucose increased NOD1 expression and decreased the level of miR-495 in human CFs. [score:3]
These findings suggest that the low level of miR-495 is closely related to the high expression of NOD1 in human CFs incubated with high glucose. [score:3]
To study the functional role of miR-495 in the regulation of pro-inflammatory cytokines affected by high glucose, we determined the mRNA and protein expressions of NOS2 and COX2 using quantitative RT-PCR and ELISA assays in high glucose-stimulated human CFs. [score:3]
CFs were transfected with miR-495 mimic for 48 h, and then treated with 5.5 or 25 mM glucose for 24 h. a The protein expressions of p-IKK, t-IKK, p-IκBα, t-IκBα, p-NF-κB, t-NF-κB, p-Smad3, t-Smad3 and PAI-1 were determined via western blot. [score:3]
Moreover, the bioinformatics analysis predicted that NOD1 was a potential target gene for miR-495. [score:3]
This level was dramatically decreased by overexpression of miR-495 (Fig.   4a). [score:3]
The introduction of miR-495 could significantly inhibit the high glucose-activated NF-κB and TGF-β1/Smad signaling pathways. [score:3]
The luciferase reporter assay, quantitative RT-PCR and western blot were used to explore whether NOD1 was a target of miR-495. [score:2]
MicroRNA-495 Human cardiac fibroblasts High glucose Cardiac fibrosis NOD1 Diabetes mellitus is a global health concern, in part due to the associated increased risk of cardiovascular disease [1]. [score:2]
The levels of NOD1 and miR-495 were then determined via quantitative RT-PCR. [score:1]
The luciferase reporter constructs with the NOD1 3’UTR carrying a putative miR-495 -binding site into the pMiR-report vector were amplified via PCR. [score:1]
Effect of miR-495 on high glucose -induced differentiation of CFs into myofibroblasts. [score:1]
Fig. 4Effects of miR-495 on high glucose -induced imbalance of MMP-TIMP and collagen synthesis in human CFs. [score:1]
The vehicle is transfection reagent alone As fibroblasts are the primary source of TGF-β in the heart and might modulate the production of extracellular matrix [20], we analyzed the TGF-β pathway in CFs treated with miR-495 and incubated with high glucose. [score:1]
Effects of miR-495 on the high glucose -induced NF-κB and TGF-β1/Smad signaling pathways. [score:1]
b The levels of miR-605, miR-924, miR-3194-3p, miR-495 and miR-4477a were determined via quantitative RT-PCR. [score:1]
In our study, introduction of miR-495 had a protective effect on CFs that were exposed to high glucose, reducing pro-inflammatory cytokines, cell differentiation and extracellular matrix accumulation. [score:1]
Our data indicate that the level of miR-495 was significantly lower in the human CFs incubated with high glucose, but other miRNAs levels did not change (Fig. 1b). [score:1]
Fig. 6The effects of miR-495 on high glucose -induced NF-κB and TGF-β1/Smad signaling pathways. [score:1]
These results showed a link between miR-495 and MMPs in cardiac fibrosis related to diabetes. [score:1]
The effects of miR-495 on the NF-κB and TGF-β1/Smad signaling pathways were also detected via western blot. [score:1]
Effect of miR-495 on high glucose -induced imbalance of MMP-TIMP and collagen synthesis in human CFs. [score:1]
Our findings suggest a critical role for miR-495 in modulating ECM remo deling in CFs exposed to high glucose. [score:1]
These results suggest that miR-495 might play an important in high glucose -induced ECM remo deling by activating the differentiation of fibroblasts into myofibroblasts. [score:1]
However, miR-495 played a protective role when introduced to CFs that were incubated with high glucose in vitro. [score:1]
Fig. 3Effects of miR-495 on high glucose -induced differentiation in human CFs. [score:1]
Fig. 2Effects of miR-495 on pro-inflammatory cytokines in human CFs incubated in high glucose. [score:1]
To the best of our knowledge, it is the first report to clarify the effects of miR-495 on the function of CFs exposed to high glucose. [score:1]
The effects of miR-495 on pro-inflammatory cytokines in human CFs incubated with high glucose. [score:1]
The vehicle is transfection reagent aloneAs fibroblasts are the primary source of TGF-β in the heart and might modulate the production of extracellular matrix [20], we analyzed the TGF-β pathway in CFs treated with miR-495 and incubated with high glucose. [score:1]
Based on our results, miR-495 could effectively prevent high glucose -induced pro-inflammatory and pro-fibrotic effects in human CFs, so the high glucose-stimulated NF-κB and TGF-β1/Smad signaling pathways were analyzed in human CFs. [score:1]
The precise molecular mechanisms and functional role of miR-495 in high glucose -induced cardiac fibrosis remain unclear. [score:1]
This shows that miR-495 plays critical roles in the pathogenesis of diabetic cardiac fibrosis and suggests that it may have applications in the treatment of cardiac fibrosis in patients with diabetes mellitus. [score:1]
Cells were co -transfected with the reporter construct, control vector or miR-495 mimic, or the corresponding controls using Lipofectamine 3000 (Invitrogen). [score:1]
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[+] score: 34
Regulation of methylation also provides an explanation for the miR-410 -mediated decrease in FHL1 both at the level of mRNA and protein, whereas two other miRNAs (miR-214, and miR-495) down-regulate FHL1 expression only at the protein level. [score:7]
These results suggest that miR-495 and miR-214 inhibit FHL1 at the protein level, but that miR-410 functions to inhibit miR-410 via a mechanism that occurs prior to FHL1 translation. [score:7]
Western blot analysis showed that miR-410, miR-495, and miR-214 could inhibit FHL1 protein expression the most dramatically (Figure. [score:5]
These data suggest that miR-410, miR-495, and miR-214 specifically inhibit the FHL1 3′UTR, but that the effects of miR-146a and miR-146b-5p may be non-specific or at sites other than their predicted target sites. [score:5]
verify that each of the 5 miRNAs could inhibit the activity for the wt-FHL1 3'UTR luciferase plasmid; however, mutation of the seed recognition sequence prevented a decrease in luciferase activity only for miR-410, miR-495 and miR-214 (Figure. [score:4]
Interestingly, FHL1 mRNA expression also was decreased by miR-410, but not miR-495 or miR-214 (Figure. [score:3]
Preliminary screening results showed that miR-146a, miR-146b-5p, miR-214, miR-495, and miR-410 can significantly inhibit luciferase activity (Figure. [score:3]
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[+] score: 21
For example, upregulated miRNAs targeted CDC7 (targeted by miR-30a-5p and miR-630) and CDK2 (targeted by miR-638), while downregulated miRNAs targeted CDKN1A (targeted by miR-299-5p), CDKN1B (targeted by miR-218-5p and miR-495-3p) and CCNA2 (targeted by miR-218-5p). [score:21]
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[+] score: 18
miR-495 is also predicted to target 6,626 different genes and has 13,900 different target sites. [score:5]
In consequence, around 60% microRNAs are predicted to have between 2,000 and 5,000 different target sites and four microRNAs (miR-495, miR-548c-3p, miR-590-3p and miR-603) are predicted to exhibit affinity towards more than 10,000 target sites – which represents around 6000 genes (Supplementary Figures S1a & S1b). [score:5]
Lastly, 7 hubs from the 11 hubs discovered by DIANA-microT are retrieved within the 40 degree sorted nodes on the TargetScan network (in decreasing order by degree: miR-548c-3p, miR-590-3p, miR-579, miR-186, miR-513a-3p, miR-661, miR-495 and lastly miR-940). [score:3]
Within this club, only miR-495 and miR-543 are clustered on the genome. [score:1]
It comprises miR-495, miR-548c-3p, miR-590-3p, miR-186, miR-579, miR-513a-3p, miR-543 and miR-944. [score:1]
These 7 microRNAs (the 3 microRNAs from the assorted club 2 and 4 from the assorted club 1, namely miR-495, miR-548c-3p, miR-590-3p and miR-186) also seem to be placed at key central positions in the network, defining two separate zones (Figure 2a). [score:1]
Nonetheless, the positions of the members of this assorted club are central to the graph, especially for miR-548c-3p, miR-590-3p, and miR-495 (Figure 2b). [score:1]
The assorted club 1 is composed of 8 microRNAs (Supplementary Table II), including the microRNA with the highest degree in the graph (miR-495). [score:1]
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[+] score: 18
Of particular interest, up-regulated miRNAs miR-494 and miR-495 were predicted to target CTNND2, while up-regulated miR-376c and miR-409-3p were predicted to target NR2F2, which were both down-regulated in primary MB specimens relative to CD133+ NSCs (Table S4). [score:14]
In particular, several miRNAs mapping to 14q32, including miR-376c, miR-495 and miR-539, were identified as up-regulated in MB specimens defined by a neuronal differentiation signature (sub-type C as per [8]) [33]. [score:4]
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[+] score: 15
miR-125a-5p and miR-125b-5p (but not miR-134-3p or miR-495-3p) altered CYP11B2 expression in vitro through direct targeting of its transcript 3′UTR. [score:6]
In order to identify individual miRNAs contributing to the net miRNA effect, as observed under Dicer1 knockdown, four miRNAs (miR-125a-5p, miR-125b-5p, miR-134-3p, and miR-495-3p) expressed in human adrenal tissue and with putative binding sites in the 3′UTR of CYP11B2 were selected for further study. [score:4]
This is borne out by the fact that qRT-PCR analysis of specific miRNA levels in the Dicer1 knockdown cells showed no significant reduction on the levels of the miRNAs miR-125a-5p, miR-125b-5p, miR-134-3p, miR-320a-3p, and miR-495-3p relative to controls (data not shown). [score:2]
Pre-miR™ or Anti-miR™ molecules (miR-125a-5p: product code 12561; miR-125b-5p miR-134-3p 10341; miR-495-3p: 11526; and miR-320a-3p: 11621, Applied Biosystems) were transfected to a final concentration of 50 nM and prevalidated siRNA molecules (Dicer 1A: product code s23755; Dicer 1B: s23756, Applied Biosystems) to a final concentration of 30 nM. [score:1]
Of the five miRNAs investigated in the current study, two (miR-125a-5p and miR-495-3p) were expressed at significantly lower levels in APA tissue relative to nontumorous tissue; one (miR-320a-3p) was significantly increased in APA tissue and two (miR-125b-5p and miR-134-3p) did not differ significantly between the tissue types (Figure 6). [score:1]
Manipulation of miR-134-3p or miR-495-3p levels in this manner did not significantly affect the luciferase activity of the pEZX-B2 reporter construct. [score:1]
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[+] score: 14
Moreover, miR-130b [99], miR-301a [100], miR-106a [101], miR-103a [102], miR-495 [103], and miR-532-5p [104] directly inhibit RUNX3 translation at the post-transcriptional level. [score:6]
In addition, increased H3K9 dimethylation and reduced H3 acetylation, as well as the increased miR-130b, miR-301a, miR-106a, miR-103a, miR-495, and miR-532-5p, synergistically inhibited the expression of RUNX3 Numerous studies have demonstrated that H. pylori infection is closely related to abnormal CpG island methylation. [score:5]
In addition, increased H3K9 dimethylation and reduced H3 acetylation, as well as the increased miR-130b, miR-301a, miR-106a, miR-103a, miR-495, and miR-532-5p, synergistically inhibited the expression of RUNX3 The exploitation of characteristic epigenetic alterations during the malignant transformation of gastric mucosa allows for the prevention, diagnosis, treatment, and prognostic evaluation of gastric cancer from a new perspective independent of protein expression. [score:3]
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[+] score: 14
We have shown the top TFs and its related diseases for rhesus inter-species in Table  5. Besides these, mml-miR-338-5p, mml-miR-218, mml-miR-495, mml-miR-203, mml-miR-590-3p, mml-miR-596, mml-miR-548p, and mml-miR-524-5p have connection with “an auto immune disease like SIV” [52], Huntintong’s Disease [53], Age mediated skeletal muscle contamination [54], Enhances Coxsackievirus B3 replication [55], Neuro inflammation Disorder [56], Schizophernia [57], monkey hippocampus effected [58], and Amyotrophic lateral sclerosis [59], respectively. [score:7]
On the other hand, as mentioned in [38], the topmost miRNA namely hsa-miR-579 has a connection with Alzheimer’s Disease; whereas the second top miRNA entitled as hsa-miR-495 relates to HIV mediated dementia [39]. [score:3]
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-524-5p and miR-495) are known (i. e., known to both human and rhesus), and remaining eight miRs (viz. [score:1]
, hsa-miR-19a and hsa-miR-495, respectively. [score:1]
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[+] score: 13
The upregulation of miR-495 in breast cancer cells was shown to suppress E-cadherin expression to promote cell invasion, and inhibit REDD1 expression to enhance cell proliferation under hypoxic conditions [16]. [score:12]
Therefore, miR-495 contributes to breast cancer cell proliferation and hypoxia resistance. [score:1]
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[+] score: 12
Fig. 1 a Correlation graph between miR-494 and miR-495 expression levels in tumor tissue from 28 randomly selected HCC patients. [score:3]
Since miR-494 and miR-495 were shown to be the most potent cluster members influencing tumor cell proliferation [18], we also analyzed miR-495 expression in HCCs. [score:3]
a Correlation graph between miR-494 and miR-495 expression levels in tumor tissue from 28 randomly selected HCC patients. [score:3]
TaqMan MicroRNA assays (Thermo Fisher Scientific) were used for quantifying miRNA-494 (ID: 002365) and miR-495 (ID:001108) expression, as previously described [8]. [score:2]
A positive correlation between miR-494 and miR-495 was found in tumors (Pearson’s correlation; p = 0.002) but not in surrounding livers (Fig.   1a, Supplementary Fig. S2A), suggesting their possible involvement in hepatocytes malignant transformation. [score:1]
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[+] score: 10
Importantly, the miRNAs miR-495-3p, miR-654-3p, miR-376a-3p and miR-487b-3p exhibited marked downregulation after 5 weeks in contrast to a slight reduction of expression observed for most miRNA genes from this region. [score:6]
The analysis of randomly-chosen miRNAs from clusters 1 and 2 (miR-654-3p, mir-369-3p, miR-495, miR-370-5p, miR-127-5p and miR-376c-3p) in tumor cell lines confirmed their downregulation (Figure 1d). [score:4]
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[+] score: 9
Similar trends were observed for miR-379, miR-494, miR-495 and miR-377, but not miR-822, suggesting that inhibition of hlnc-MGC (host RNA) by HMGC10 reduces the cluster miRNAs in HMC treated with TGF-β1 (Fig. 8a). [score:3]
TGF-β1 and HG significantly increased the expression of miR-379, miR-494, miR-495 and miR-377 as well as lnc-MGC, but not miR-882, compared with serum depleted (SD) or normal glucose (NG) controls respectively in cultured mouse MC (MMC; Fig. 2d). [score:2]
Mir-495 and -377 as well as Mirg levels were also inhibited (Supplementary Fig. 21f–i). [score:2]
The increases of lnc-MGC, miR-379, miR-494, miR-495 and miR-377 noted in glomeruli from diabetic WT mice were not observed in glomeruli from diabetic Chop- KO mice (five mice in each group). [score:1]
miR-379 is located at the 5′ end, miR-494 and miR-495 in the middle, and miR-377 downstream (Fig. 1c). [score:1]
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[+] score: 8
For example, Lee and colleagues showed that the combination of miR-130a and miR-495 produced a greater decrease in the expression of the tumor suppressor RUNX3, than either miRNA alone [18]. [score:5]
Targeting of RUNX3 by miR-130a and miR-495 cooperatively increases cell proliferation and tumor angiogenesis in gastric cancer cells. [score:3]
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[+] score: 8
MiR-495 regulates proliferation and apoptosis in HUVECs by targeting the chemokine CCL2 [15]. [score:3]
Liu D. Zhang X. L. Yan C. H. Li Y. Tian X. X. Zhu N. Rong J. J. Peng C. F. Han Y. L. MicroRNA-495 regulates the proliferation and apoptosis of human umbilical vein endothelial cells by targeting chemokine CCL2 Thromb. [score:3]
Furthermore, several other microRNAs are also shown to be important in regulating endothelial cell apoptosis, including miR-19a, miR-26a, miR-495, miR-US25-1, miR-223, let-7, miR-126, miR-21, miR-590-5p, miR-513a-5p, miR-23a, miR-365, etc. [score:2]
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[+] score: 8
Other miRNAs from this paper: hsa-mir-127, hsa-mir-154, hsa-mir-376c, hsa-mir-494, hsa-mir-496
Based on the qRT-PCR results, the hESCs with higher MEG3 and MEG8 expression were classified as MEG3-ON hESCs, in which several miRNAs from this locus, miR-127-3p, miR-154, miR-376c, miR-494, miR-495, and miR-496, were also abundantly expressed (Figure  1B). [score:5]
The UPL probe system (Roche) was used to detect the expression of miRNAs, including miR-127-3p, miR-376c, miR-494, miR-495, miR-496, and miR-154. [score:3]
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[+] score: 7
Although our analysis does not extend to include fully functioning islets, we did detect increased expression of miR-127-3p and miR-495 at day 8 and day 11. miR-184 was also detected at high levels at day 11 relative to the day 1– day 8 samples, but we also observed high expression in the starting hESC population, suggesting that although it may have a role in development it is not islet-specific. [score:6]
A recent study by Bolmeson et al., of miRNA enriched in pancreatic islet samples versus liver and skeletal muscle identified miR-127-3p, miR-184, miR-195 and miR-495 [28]. [score:1]
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[+] score: 7
As expected, miR-206 (p = 0.0001; Mann–Whitney test), miR-129-5p (p = 0.002), miR-323-3p (p = 0.014), and miR-495 (p = 0,054), had lower expression in MB in comparison to normal cerebellum (Figure 3), thus confirming our microarray findings. [score:3]
Expression of miR-495 was not performed in D341 cell line. [score:3]
73(12) hsa-miR-377* 14q32.2 −2.72 hsa-miR-7 15q25.3/19p13.3/9q21.32 −2.72(12, 14) hsa-miR-124 20p23.1/8q12.3/8p23.1 −2.71(12, 14, 29, 48, 49) hsa-miR-323-5p 14q32.31 −2.69(12) hsa-miR-873 9p21.1 −2.65 hsa-miR-129* 11p11.2/7q32.1 −2.63 hsa-miR-338-5p 17q25.3 −2.61(14) hsa-miR-409-5p 14q32.2 −2.61 hsa-miR-874 5q31.2 −2.46 hsa-miR-495 14q32.2 −2.46(52) hsa-miR-885-5p 3p25.3 −2.45 hsa-miR-376c 14q32.2 −2.43(52) hsa-miR-299-5p 14q32.2 −2.41 hsa-miR-539 14q32. [score:1]
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[+] score: 7
The study also indicated that miR-495, miR-433, and miR-410 levels can be used to predict both disease free survival (DFS) and OS in gastric cancer patients [104]. [score:3]
The methylation pattern in the MEG3 DMR as well as the expression profile of miRNAs in the region can distinguish high-aggressiveness versus low-aggressiveness osteosarcoma cell lines, and the levels of miR-495, miR-329, miR-487b, miR-410, and miR-656 can predict the outcome of patients with osteosarcoma [107]. [score:3]
In addition, miR-495, miR-134, miR-409-3p, miR-496, miR-379, miR-369-3p in the cluster are linked to the tumor invasion depth in gastric cancer [104, 106]. [score:1]
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[+] score: 7
Remarkably, MeCP2 silences miR-30a/d, miR-381 and miR-495, which in turn repress Brain-derived neurotrophic factor (BDNF), the down-regulated target gene in Mecp2 -null mice (Wang et al., 2006); this suggests a multilayered MeCP2 -mediated transcriptional regulation of BDNF (Wu et al., 2010). [score:7]
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[+] score: 6
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-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-217, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-328, hsa-mir-335, hsa-mir-133b, hsa-mir-409, hsa-mir-484, hsa-mir-485, hsa-mir-486-1, hsa-mir-490, hsa-mir-193b, hsa-mir-497, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-506, hsa-mir-509-1, hsa-mir-532, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-33b, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-1224, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-802, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-4262, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, 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-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, 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-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-486-2, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
The ethanol -induced decrease in miR-26a and miR-495 was suggested to increase target mRNAs, brain-derived neurotropic factor (BDNF) and SIRT1, a protein deacetylase [119]. [score:3]
Rats exposed to acute-binge ethanol during puberty showed decreased expression of miR-26a and miR-495 in the dorsal and ventral hippocampus [119]. [score:3]
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[+] score: 6
In an attempt to discover whether the guinea pig Abcb1 isoform 1’s 3′UTR contains MREs, the reverse complement of several human ABCB1-specific miRs validated to reduce ABCB1 mRNA expression and ABCB1 activity (miR223 [24], miR508-5p [25], bta-miR145 [26], miR381 and miR-495 [27]) were searched via BLAST alignment for extrapolation to guinea pig; however, none were found. [score:3]
The human miR cluster at 14q32.31, an imprinted region, containing miR-381 and miR-495, contains over 20 miR sequences, several known to inhibit ABCB1 in human, and there is 90% homology (BLAT) between this region and a 31 kb region in the guinea pig genome, on the plus strand of scaffold 111, therefore representing a candidate region for miR discovery. [score:3]
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[+] score: 6
The boxplots show the expression levels of miR-197-5p (a), miR-4697-5p (b), miR-4721 (c), miR-5006-5p (d), miR-575 (e), miR-6893-5p (f), miR-125a-5p (g), miR-1260b (h), miR-224-3p (i), miR-331-3p (j), miR-365a-3p (k), miR-495-3p (l), miR-518b (m), miR-518f-3p (n), miR-543 (o) and miR-7977 (p). [score:3]
Nine (miR-125a-5p, miR-224-3p, miR-331-3p, miR-365a-3p, miR-495-3p, miR-518b, miR-518f-3p, miR-543, and miR-7977) were significantly downregulated in FET placentae compared with SP, but not ET (Fig. 2 and Additional file 5: Figure S1). [score:3]
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[+] score: 5
Both miR-145 and miR-495 target SOX9 in mesenchymal stem cells (9, 28), and miR-101 targets SOX9 in hepatocellular carcinoma (29). [score:5]
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[+] score: 4
Li et al. [30] discovered that miRNA-495 down-regulates PRL-3 mRNA and protein levels in gastric cancer cells. [score:4]
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[+] score: 4
According to the study conducted by Mo and colleagues, human ESCs with low MEG3 expression level (designated as MEG3-OFF) also showed significantly low expressions of DLK1-DIO3 locus-derived noncoding RNAs, including MEG8, miR-127, miR-376, miR-494, miR-495, miR-496, and miR-154, compared to its counterpart MEG3-ON [68]. [score:4]
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[+] score: 4
MicroRNAs including miR-125a/b, miR-495 and miR-181 have been shown to be dysregulated in a variety of neurological disorders such as Alzheimer’s disease. [score:4]
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[+] score: 4
MiR-495 inhibits chondrogenesis in human MSCs by targetting SRY-box 9 (Sox9) [30]. [score:4]
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[+] score: 4
miR-495 and miR-551a inhibit the migration and invasion of human gastric cancer cells by directly interacting with PRL-3. Cancer Lett. [score:4]
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[+] score: 4
Several microRNAs (miRNAs) including Let-7b, miR-495, and miR-18a are also essential in regulating acinar cell differentiation and homeostasis by modulating the expression of transcription factors [98, 99]. [score:4]
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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
The largest decreases in expression occurred in miR-636 and miR-495-3p at 2.423 and 1.62 fold of the control level, respectively. [score:3]
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[+] score: 3
Other miRNAs from this paper: mmu-mir-495
Subsequent to obtaining these expression results, comparative genomic investigation using the UCSC genome browser and focused on the 3′ untranslated region (UTR) of human MAOA revealed the presence of a microRNA binding site for a human-mouse conserved microRNA (miR-495, chrX:43606034–43606041). [score:3]
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[+] score: 3
Our computational study states that the elevated level of miR-1252, miR-4697, miR-4724, and miR-495, negatively regulates the STAT1 signaling. [score:2]
By using all three web servers, miR-1252, miR-4697, miR-4724, and miR-495 were found to be potential miRNA against STAT1 gene. [score:1]
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[+] score: 3
Welten SMJ Inhibition of 14q32 MicroRNAs miR-329, miR-487b, miR-494, and miR-495 increases neovascularization and blood flow recovery after ischemiaCirc. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-329-1, hsa-mir-329-2, hsa-mir-543
An example is miR-329 family, in which any pairs of the three members (i. e. hsa-mir-543, hsa-mir-329, hsa-mir-495) share less than 20% of the targets. [score:3]
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[+] score: 3
Similarly, longSAGE tags also suggest the expression of two human (mir-7-1 and mir-125a) and three mouse (mir-331, mir-351, and mir-495) miRNAs that have not been experimentally confirmed (Table 1). [score:3]
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[+] score: 2
RNA was isolated on two separate occasions following the miRVana protocol from the frontal cortex tissue and subjected to RT-PCR for miR122 (diamond), miR125a-3p (square), miR132 (triangle), and miR134 (X), and miR495 (asterisk). [score:1]
The following RNAs (Applied Biosystems product ID#s) were analyzed: MammU6 (#4395470), RNU44 (#4373384), miR-122 (#4395356), miR-29a (#4395223), miR-367 (#4373034), miR-142-5p (#4395359), miR-154 (#4373270), miR-214 (#4395417), miR-193a-3p (#4395361), miR-495 (#4381078), miR-125a-3p (#4395310), miR-134 (4373143). [score:1]
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[+] score: 2
For example, we showed that changes in plasma exosomal miRNA (miR-9, miR-181c, miR-495, miR-599) that are known to regulate fibrosis, cardiomyocyte energetics, and mitochondrial function are detected in dogs with MMVD and CHF [12]. [score:2]
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[+] score: 2
Formosa A, Markert EK, Lena AM, Italiano D, Finazzi-Agro E, Levine AJ, et al. s, miR-154, miR-299-5p, miR-376a, miR-376c, miR-377, miR-381, miR-487b, miR-485-3p, miR-495 and miR-654-3p, mapped to the 14q32.31 locus, regulate proliferation, apoptosis, migration and invasion in metastatic prostate cancer cells. [score:2]
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[+] score: 2
Gene Name Protein Name Consensus Results CASP9 Caspase-9 hsa-miR-124 hsa-miR-182 hsa-miR-504 hsa-miR-506 hsa-miR-96 RIPK2 Receptor-interacting serine/threonine-protein kinase 2 hsa-miR-200b hsa-miR-200c GRB2 Growth factor receptor-bound protein 2 hsa-miR-182 CDK2 Cyclin -dependent kinase 2 hsa-miR-200b hsa-miR-200c hsa-miR-429 CASP8 Caspase-8 hsa-miR-17 hsa-miR-20b hsa-miR-495 hsa-miR-519d hsa-miR-93 RAF1 Rapidly Accelerated Fibrosarcoma (RAF) proto-oncogene serine/threonine-protein kinase hsa-miR-15a hsa-miR-15b hsa-miR-16 hsa-miR-195 hsa-miR-424 hsa-miR-497 With the development of systems biology, carcinogenesis could be interpreted as the malfunction of perturbed protein functional interaction networks in a cell, and therefore, analyses of apoptosis-related network from a systems-level perspective is of great significance [29, 30, 31]. [score:2]
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[+] score: 2
Using the same method to define hubs, we identified four hub genes (NRP1, FOXO3, SMAD4, and TNFRSF1B), six hub miRNAs (miR-495, miR-9, miR-137, miR-30d, miR-181c, and miR-30e), and three hub TFs (TEAD1, SP1, and ZBTB7A). [score:1]
Accordingly, we identified 15 hub genes (FOXO3, SMAD4, TCF12, BCL11A, PDGFRA, KLF4, NRAS, SOX11, CACNA1E, ELAVL2, PIK3R1, RPS6KA3, SLC9A2, CYLD, and PTCH1), 4 hub miRNAs (miR-9, let-7i, miR-495 and miR-130a) and 6 hub TFs (TEAD1, SP1, MZF1, NEUROD1, GATA1, and TCF7). [score:1]
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[+] score: 2
We received a notably reduced list containing 7 miRs (hsa-miR-144, hsa-miR-101, hsa-miR-375, hsa-miR-200a, hsa-miR-183, hsa-miR-495, hsa-miR-222) with a potential role in CAKUT development. [score:2]
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[+] score: 2
Our results also suggest the involvement of miR-127, miR-27b, miR-30b, miR-655, miR-95 and miR-495 in skeletal muscle development (S1B Fig. ). [score:2]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-376c, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-342, hsa-mir-151a, hsa-mir-324, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-576, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-411, hsa-mir-671, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-885, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
An miRNA pairwise approach has demonstrated the potential use of two pairs of plasma miRNAs as biomarkers for cognitive-impaired HIV -positive individuals: miR-495-3p in combination with let-7b-5p, miR-151a-5p, or miR-744-5p; and miR-376a-3p/miR-16-5p (211). [score:1]
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[+] score: 1
According to miRBase annotation, hsa-mir-1277, hsa-mir-376a-2, hsa-mir-495, hsa-mir-659, hsa-mir-1303, hsa-mir-1307 and so on encode mature miRNA at only their 3p arms. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-18a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-21, hsa-mir-23a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-98, hsa-mir-99a, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-99a, mmu-mir-127, mmu-mir-128-1, mmu-mir-136, mmu-mir-142a, mmu-mir-145a, mmu-mir-10b, mmu-mir-182, mmu-mir-183, mmu-mir-187, mmu-mir-193a, mmu-mir-195a, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-139, hsa-mir-10b, hsa-mir-182, hsa-mir-183, hsa-mir-187, hsa-mir-210, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-224, hsa-mir-200b, mmu-mir-302a, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-128-1, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-127, hsa-mir-136, hsa-mir-193a, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, 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-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-96, mmu-mir-98, hsa-mir-200c, mmu-mir-17, mmu-mir-139, mmu-mir-200c, mmu-mir-210, mmu-mir-216a, mmu-mir-219a-1, mmu-mir-221, mmu-mir-222, mmu-mir-224, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-200a, hsa-mir-302a, hsa-mir-219a-2, mmu-mir-219a-2, hsa-mir-363, mmu-mir-363, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-18b, hsa-mir-20b, hsa-mir-452, mmu-mir-452, ssc-mir-106a, ssc-mir-145, ssc-mir-216-1, ssc-mir-217-1, ssc-mir-224, ssc-mir-23a, ssc-mir-183, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-128-1, ssc-mir-136, ssc-mir-139, ssc-mir-18a, ssc-mir-21, hsa-mir-146b, hsa-mir-493, hsa-mir-497, hsa-mir-505, mmu-mir-20b, hsa-mir-92b, mmu-mir-302b, mmu-mir-302c, mmu-mir-302d, hsa-mir-671, mmu-mir-216b, mmu-mir-671, mmu-mir-497a, mmu-mir-495, mmu-mir-146b, mmu-mir-708, mmu-mir-505, mmu-mir-18b, mmu-mir-493, mmu-mir-92b, hsa-mir-708, hsa-mir-216b, hsa-mir-935, hsa-mir-302e, hsa-mir-302f, ssc-mir-17, ssc-mir-210, ssc-mir-221, mmu-mir-1839, ssc-mir-146b, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-128-2, ssc-mir-143, ssc-mir-10b, ssc-mir-23b, ssc-mir-193a, ssc-mir-99a, ssc-mir-98, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-142, ssc-mir-497, ssc-mir-195, ssc-mir-127, ssc-mir-222, ssc-mir-708, ssc-mir-935, ssc-mir-19b-2, ssc-mir-19b-1, ssc-mir-1839, ssc-mir-505, ssc-mir-363-1, hsa-mir-219b, hsa-mir-371b, ssc-let-7a-2, ssc-mir-18b, ssc-mir-187, ssc-mir-218b, ssc-mir-219a, mmu-mir-195b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-31, ssc-mir-182, ssc-mir-216-2, ssc-mir-217-2, ssc-mir-363-2, ssc-mir-452, ssc-mir-493, ssc-mir-671, mmu-let-7k, ssc-mir-7138, mmu-mir-219b, mmu-mir-216c, mmu-mir-142b, mmu-mir-497b, mmu-mir-935, ssc-mir-9843, ssc-mir-371, ssc-mir-219b, ssc-mir-96, ssc-mir-200b
Of the miRNAs in the porcine Dik1-Dio3 region, there were four annotated miRNAs: ssc-miR-127, ssc-miR-495, ssc-miR-493 and ssc-miR-136. [score:1]
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[+] score: 1
This cluster included miR-495, miR-376a, and miR-369-5p. [score:1]
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[+] score: 1
Consistent with the interspecies shift based on PC2, 3 out of the first 5 implicated miRNAs (miR-411, miR-410, miR-382, miR-495 and miR-494) were differentially modulated in human and mouse samples (Table 1). [score:1]
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[+] score: 1
In the Hh signalling pathway, we detected mir-495 and mir-383 for Gas1 and mir-654-5P for Gli3. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-519a-1, hsa-mir-519a-2
Of note, a test for “hits” that also have activity against the recent pandemic strain Cal/04/09 identified two miRNA mimics that impair Cal/04/09 protein production in A549 cells (hsa-miR-495 and hsa-miR-519a, Figure 6D). [score:1]
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