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41 publications mentioning hsa-mir-362

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-362. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 210
Following the nucleofection -mediated transfection of primary pNK cells with an FAM -labelled miR-362-5p inhibitor, the expression of miR-362-5p was downregulated to some degree in the miR-362-5p inhibitor -transfected pNK cells (Fig. 6a). [score:10]
Because miRNAs function primarily through the inhibition of target genes, we next sought to identify the mRNA targets regulated by miR-362-5p in human NK cells that might be involved in human NK cell function. [score:8]
Because miR-362-5p was upregulated in human primary pNK cells (Fig. 3d), we used nucleofection to knock down miR-362-5p with miR-362-5p inhibitors and measured CYLD expression in pNK cells. [score:7]
An expanded analysis of 955 different miRNAs across 5 human lymphocyte subsets revealed that, although there were other differentially expressed miRNAs upregulated in NK cells compared with NKT and T cells (Figs. 1e and 1f), miR-362-5p was the only miRNA that was specifically upregulated by more than 10-fold in human pNK cells compared with dNK cells, a finding that was confirmed by qRT-PCR (Fig. 3d and Supplementary Fig.  S2). [score:7]
Because miR-362-5p was downmodulated in human primary dNK cells (Figs. 1f and 3d), we assessed the direct regulation of CYLD expression as a result of miR-362-5p overexpression in dNK cells. [score:7]
To validate the microarray data, we selected 3 miRNAs (miR-10b-5p, miR-1471 and miR-199a-5p) that were downregulated in pNK cells and 3 miRNAs (miR-181a-2-3p, miR-26b-3p and miR-362-5p) that were upregulated in human pNK cells for RT-PCR confirmation. [score:7]
To experimentally verify CYLD as a target of miR-362-5p in human NK cells, we examined the effect of miR-362-5p overexpression on endogenous CYLD expression. [score:7]
Moreover, we demonstrated that miR-362-5p acts as a positive regulator of NK cell function by upregulating the expression of IFN-γ, granzyme-B, and perforin and enhancing the degranulation of NK cells in humans. [score:7]
Furthermore, we found by quantitative real-time PCR and flow cytometric analysis that the expression of perforin, granzyme-B, and IFN-γ was also significantly decreased in the above miR-362-5p inhibitor -transfected pNK cells compared with the pNK cells transfected with a control inhibitor (synthetic RNA with a random sequence; Figs. 6b and 6c). [score:6]
Although we do not have direct evidence that miR-362-5p influences NK cell function through NF-κB signaling pathway, this hypothesis is supported by the observation that IFN-γ production was significantly decreased by an NF-κB inhibitor in both control and miR-362-5p overexpressing NK cells. [score:6]
In this study, we showed that knockdown of CYLD by siRNA mirrored the effect of miR-362-5p over -expression and resulted in significantly increased perforin, granzyme B, IFN-γ and CD107a expression in human NK cells. [score:6]
We found that the overexpression of miR-362-5p resulted in significantly increased CD107a expression (Fig. 5f). [score:5]
We assessed the inhibitory effect of miR-362-5p on 5 putative target genes relative to NK cell function. [score:5]
Red and green pseudocolors indicate transcripts levels below or above the mean, respectively, on a log 2 scale representing gene expression ratios from 0 to 6. (c) Real-time PCR analysis of the expression of miR-10b-5p, miR-1471, miR-199a-5p, miR-181a-2-3p, miR-26b-3p, and miR-362-5p. [score:5]
We used TargetScan to make bio-informative predictions of the potential miR-362-5p target genes. [score:5]
Inhibition of miR-362-5p acts through CYLD to suppress human NK cell function. [score:5]
In addition, we revealed that a novel miRNA, miR-362-5p, was highly expressed in human pNK cells where it promoted NK cell effector function by targeting CYLD. [score:5]
MiR-362-5p directly regulates CYLD expression in human NK cells. [score:4]
Our data suggest that miR-362-5p promotes the effector function of human NK cells, at least in part, through the down-regulation of CYLD. [score:4]
To confirm our hypothesis, we transfected CYLD siRNA into the anti-miR-362-5p -transfected pNK cells to knockdown CYLD expression. [score:4]
However, our data analysis identified several miRNAs, such as miR-362-5p, that were up-regulated in pNK cells and are associated with the function of human NK cells. [score:4]
We further demonstrated that mutation of the miR-362-5p-responsive elements in the CYLD 3′ UTR resulted in the abrogation of the inhibitory effect of miR-362-5p (Figs. 4b and 4c). [score:4]
Collectively, the above results suggest that miR-362-5p directly targets CYLD in human NK cells. [score:4]
A corollary of our hypothesis that miR-362-5p promotes human NK cell effector function by targeting CYLD is that knockdown of CYLD will enhance NK cell function. [score:4]
These stringent criteria were met by 7 miRNAs that were specifically up-regulated in NK cells compared to NKT and T cells (miR-340-3p, miR-210, miR-199a-3p, miR-483-3p, miR-130a-3p, miR-199b-5p, and miR-362-5p) (Fig. 1e). [score:3]
As shown in Supplementary Fig.  S4, miR-362-5p overexpression dramatically enhanced the cytokine -induced IFN-γ production of dNK cells, and this enhancement was attenuated by PDTC. [score:3]
We demonstrated above that the overexpression of miR-362-5p promotes human NK cell effector function in human NK cells. [score:3]
When transfected with a miR-362-5p inhibitor (anti-miR-362-5p), human primary pNK cells showed a dramatic decrease in their cytotoxic activity and a CD107a release (Figs. 6d and 6e). [score:3]
A fragment of the 3′ UTR of CYLD DNA containing the wild-type or mutated target sequence of miR-362-5p was inserted into the digested psiCHECK-2 vectors (Promega). [score:3]
Figs. 4d and 4e indicate a significant reduction in CYLD mRNA and protein levels in human dNK cells after miR-362-5p overexpression. [score:3]
We found that miR-362-5p directly regulated 2 of the 5 3′ UTRs (Fig. 4a). [score:3]
Synthetic miR-362-5p mimics, miR-362-5p inhibitors, CYLD siRNAs, and negative controls were all purchased from GenePharma. [score:3]
The knockdown of CYLD led to an increase in NK cell function compared with the scramble controls, mirroring the phenotype observed with the overexpression of miR-362-5p (Figs. 5i, 5j and 5k). [score:3]
To ascertain whether the NF-κB signaling pathway is responsible for the increased function of miR-362-5p -transfected NK cells, we pretreated control and miR-362-5p -transfected dNK cells with pyrrolidine dithiocarbamate (PDTC, a specific inhibitor of NF-κB) before cytokine stimulation. [score:3]
We hypothesized that increased CYLD levels may mediate the inhibitory effect of miR-362-5p. [score:3]
The transfection efficiency of the FAM-labeled-miR-362-5p mimics or inhibitors in human NK cells is shown in Supplementary Fig.  S6. [score:3]
The overexpression of miR-362-5p resulted in a substantial increase in the cytotoxic activity of dNK cells (Fig. 5g). [score:3]
Compared with the negative control miRNA, the use of nucleofection to upregulate miR-362-5p with miR-362-5p mimics caused a significant increase in effector function in human dNK cells, as demonstrated by their higher production of perforin, granzyme B and IFN-γ (Figs. 5b, 5c and 5d). [score:3]
Purified human dNK cells transfected with miR-362-5p mimics expressed substantially more miR-362-5p than cells transfected with negative control miRNA (Fig. 5a). [score:3]
Overexpression of miR-362-5p promotes human NK cell effector function. [score:3]
To further illustrate the mechanism underlying the positive regulation of NK cell effector function by miR-362-5p, we examined the impact of miR-362-5p on NF-κB activation by detecting the level of nucleus NF-κB P65 protein in human dNK cells transfected with miR-362-5p mimics. [score:2]
These results suggested that miR-362-5p acts through the CYLD pathway to regulate NK cell function. [score:2]
To further assess whether miR-362-5p regulates cytotoxicity, purified dNK cells were transfected with either a miR-362-5p mimic or a control miRNA for 20 h. Cytotoxicity against the K562 leukemia cell line was assessed by FACS. [score:2]
The expression levels of the examined receptors were almost all increased in dNK cells transfected with miR-362-5p mimics compared with the control cells (Fig. 5e). [score:2]
Overall, these data suggest that miR-362-5p is a critical positive regulator of NK cell function. [score:2]
MiR-362-5p targets CYLD in human NK cells. [score:2]
MiR-362-5p is highly expressed in human pNK cells. [score:2]
The knockdown of miR-362-5p led to a substantial increase in CYLD mRNA and protein levels in human primary pNK cells (Figs. 4f and 4g). [score:2]
Thus, it is likely that miR-362-5p enhances IFN-γ production in NK cells by regulating the NF-κB pathway. [score:2]
The HEK293T cells were transfected with 10 ng each of psi-CHECK-2 construct along with 15 pmol of the miR-362-5p mimic or an identical amount of the negative control miRNA using Lipofectamine 2000 (Invitrogen). [score:1]
Next, we studied the functional role of miR-362-5p in modulating human NK cell function by a gain-of-function approach. [score:1]
We cloned the 3′ UTRs of these genes into the psi-CHECK2 vector and co -transfected the resulting vectors into HEK293T human epithelial cells along with synthetic mature miR-362-5p double-stranded RNA (Synth miR-362-5p) or a control miRNA with a scrambled sequence (Scr ctrl). [score:1]
Taken together, these results support the conclusion that miR-362-5p promotes human NK function, at least in part, through increased activation of the NF-κB pathway. [score:1]
Next, we examined the effect of miR-362-5p loss of function on the cytotoxic activity of human NK cells. [score:1]
Because cytotoxicity and cytokine production are major functions of NK cells, we investigated the levels of the cytotoxic effector genes perforin and granzyme B and of the cytokine interferon-γ (IFN-γ) to determine whether NK cell effector function was affected by the increased miR-362-5p expression. [score:1]
Furthermore, we used qRT-PCR to verify that miR-362-5p was highly specific for human pNK cells. [score:1]
Thus, we focused on miR-362-5p and hypothesized that this novel miRNA contributes to human NK cell biology. [score:1]
[1 to 20 of 57 sentences]
[+] score: 36
A comparison was performed between the miRNAs upregulated in both MMTBI and STBI group which identified a signature of 10 miRNAs viz miR-151-5p, miR-195, miR-20a, miR-328, miR-362-3p, miR-30d, miR-451, miR-486, miR-505* and miR-92a, with increased expression in both MMTBI and STBI groups (Fig. 2, Common miRNAs in MMTBI and STBI are highlighted in bold in Tables 1 and 2). [score:6]
Validation in CSF samples showed that expression of miR-328, miR-362-3p miR-486 and miR-451 was significantly upregulated, however; no significant elevation in levels of miR-151-5p, miR-30d and miR-20a was detected. [score:6]
Moreover, the Ct values in control group for miR-362-3p were found to be very high (>35) suggesting their expression in control samples is negligible, however in injury groups their expression level considerably increased, which resulted in very high fold changes over the control. [score:5]
This analysis identified 30 genes as direct targets for the 8 miRNA candidate miR-151-5p, miR-195, miR-328-3p, miR-362-3p, miR-30d, miR-20a, miR-486 and miR-92a. [score:4]
Normalization with miR-202 showed a significant upregulation of miR-328, miR-362-3p, miR-451 and miR-486 (Fig. 4). [score:4]
MiR-151-5p and miR-362-3p target molecule SCN4A which is shown to be responsible for generation and propagation of neurons. [score:3]
We randomly selected five miRNAs miR-195, miR-328, miR-362-3p, miR-486 and miR-505* and performed specific miRNA assays to validate their expression. [score:2]
The AUC’s were: miR-195 (0.81), miR-30d (0.75), miR-451 (0.82), miR-328 (0.73), miR-92a (0.86), miR-486 (0.81), miR-505 (0.82), miR-362 (0.79), miR-151 (0.66), miR-20a (0.78). [score:1]
Comparison of miRNAs modulated in this study with that of serum miRNA from blast induced MMTBI in rats show common miRNAs such as miR-20a, miR-362-3p, miR-195, miR-451 and miR-92a. [score:1]
The real time data for miR-151-5p, miR-195, miR-20a, miR-30d, miR-328, miR-362-3p, miR-451, miR-486, miR-505* and miR-92a was normalized using miR-202. [score:1]
There were significant differences between the two groups for all but two of the selected miRNA (see asterisks): miR-195 (p < 0.001); miR-30d (p < 0.001); miR-451 (p < 0.011); miR-328 (p = 0.101); miR-92a (p < 0.001); miR-486 (p = 0.006); miR-505 (p = 0.008); and miR-362 (p = 0.035); miR-151 (p = 0.065); and miR-20a (p = 0.012). [score:1]
The analysis identified the AUC values as miR-195 (0.81, p value < 0.003), miR-30d (0.75, p value < 0.016), miR-451 (0.82, p value < 0.002), miR-328 (0.73, p value < 0.030), miR-92a (0.86, p value < 0.001), miR-486 (0.81, p value < 0.003), miR-505 (0.82, p value < 0.002), miR-362 (0.79, p value < 0.006), miR-151 (0.66, p value < 0.123), miR-20a (0.78, 0.007). [score:1]
There were significant differences between the two groups for all but two of the selected miRNA: miR-195 (p < 0.001); miR-30d (p < 0.001); miR-451 (p < 0.011); miR-328 (p < 0.101); miR-92a (p < 0.001); miR-486 (p < 0.006); miR-505 (p < 0.008); and miR-362 (p < 0.035); miR-151 (p < 0.065); and miR-20a (p < 0.012) (Fig. 5). [score:1]
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[+] score: 23
Some of the miRNAs hosted in the CLCN5 gene have also been related to cancer, e. g., high expression of miR-362 is associated to worse prognosis and apoptosis resistance in colorectal and gastric cancer [45, 46], that of miR-500a to hepatocellular carcinoma [47], and that of miR-502 to diverse types of cancer through a polymorphism in its target gene SET8 [48], and to colon cancer by inhibiting autophagy [49]. [score:7]
The ANOVA test with post hoc analysis for condition IL-4 vs conditions Pre and Ctrl identified 7 mature miRNAs regulated by IL-4 in CLL (Fig 2A and S6 Table): miR-21-3p, miR-362-3p, miR-362-5p, miR-500a-3p, miR-502-3p, miR-532-3p, and miR-532-5p, all of them higher than 10-fold up-regulated on average. [score:5]
MiR-21, miR-362, miR-500a, miR-502, and miR-532 were induced by IL-4, likely as a consequence of up-regulation of their respective host genes, vacuole membrane protein 1 (VMP1), and chloride channel, voltage sensitive 5 (CLCN5). [score:4]
We have found up-regulation of miR-21 (5p and 3p), miR-362 (3p and 5p), miR-500a-3p, miR-502-3p, and miR-532 (3p and 5p) by IL-4 in CLL. [score:4]
MiR-21 maps several hundred base pairs downstream of the last exon of VMP1, and miR-362, miR-500a, miR-502, and miR-532 within the third intron of CLCN5. [score:1]
For miRNA expression, RNA samples were retrotranscribed with the miScript II RT Kit (Qiagen) using the miScript HiSpec buffer for mature miRNA detection only, followed by qPCR with the miScript SYBR Green PCR Kit (Qiagen) in an ABI Prism 7000 Sequence Detection System, using the miScript primer assays (Qiagen) for miR-21-3p, miR-362-3p, miR-362-5p, miR-500a-3p, miR-502-3p, miR-532, miR-532-3p, and RNU6-6P, the latter used as reference for normalization (cat. [score:1]
In contrast, the levels of cytoprotection correlated significantly with the levels of change of miR-21-5p, miR-362-5p, and miR-500a-3p (Table 3), providing additional evidence to suggest that these miRNAs could play a role in the anti-apoptotic response induced by IL-4 in CLL. [score:1]
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[+] score: 17
E2F1 was regulated by miR-362, and it was also suppressed by COPS2, a targetgene of miR-181a. [score:6]
miR-362 had the least number of targetgenes, which were PTPN1 and E2F1. [score:3]
miR-362, miR-133a, and miR-122 had no targetgenes in the three pathways. [score:3]
Of these, 7 miRNAs (hsa-mir-122, hsa-mir-124, hsa-mir-133a, hsa-mir-145, hsa-mir-155, hsa-mir-181a, and hsa-mir-362) could predict targetgenes in all the three databases. [score:3]
Therefore, the correlations among SIRT1, E2F1, and COPS2 constructed a bridge between miR-362 and miR-181a. [score:1]
A total of 11 miRNAs (hsa-mir-122, hsa-mir-124, hsa-mir-133a, hsa-mir-145, hsa-mir-155, hsa-mir-181a, hsa-mir-298, hsa-mir-362, hsa-mir-497, hsa-mir-1, and hsa-let-7f) were identified to be related to human stroke based on the HMDD. [score:1]
[1 to 20 of 6 sentences]
[+] score: 10
Other miRNAs from this paper: hsa-mir-188, hsa-mir-346, hsa-mir-300
confirmed an upregulation of miR-300 in the YFP+ (CPC-B+) population, but not miR-188 or miR-362, which were not overrepresented in the YFP− population (Figure 1f). [score:4]
The expression profile of three miRNAs, miR-300, miR-188, and miR-362, was validated by RT-qPCR, but miR-346 was not confirmed (Figure 1d). [score:3]
The expression profile of the three confirmed miRNAs in CPCs corresponded to miR-362>miR-188>miR-300 (Supplementary Figure S3b). [score:3]
[1 to 20 of 3 sentences]
[+] score: 9
Other miRNAs from this paper: hsa-mir-223, hsa-mir-483
Studies have also shown that miR-362-5p facilitates the function of NK cells by downregulating deubiquitinating enzyme CYLD expression (17). [score:6]
This approach has led to the discovery of the inhibitory miRNA miR-483-3p (16) and the activated miRNA miR-362-5p (17) in human NK cells (Table 1). [score:3]
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[+] score: 9
In GC, oncogenic miRNAs such as miR-21 [12], miR-362 [13] and miR-296-5p [14] are abnormally upregulated, and tumor suppressing miRNAs such as miR-506 [15], miR-129-5p [16] and miR-361-5p [17] are significantly downregulated. [score:9]
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[+] score: 9
were chosen from GO annotations in which target genes were significantly enriched (−log [10](P-value) > 5), which included hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p. [score:3]
The five potential candidate miRNAs (hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p) may be important factors related to BSS in DM and can be used as biomarkers for diagnosis and drug targets for treating DM with BSS. [score:3]
Their miRNAs were selected as the potential candidate miRNAs of BSS in DM, which were hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p (Table 4). [score:1]
Based on the analysis, it showed that five miRNAs were closely related to BSS in DM, including hsa-miR-140-5p, hsa-miR-210, hsa-miR-362-5p, hsa-miR-590-3p, and hsa-miR-671-3p. [score:1]
A study to evaluate miRNA involvement in gestational diabetes mellitus (GDM) discovered that miR-362-5p was significantly down-regulated in GDM, compared with normal controls [46]. [score:1]
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[+] score: 8
RT-qPCR was performed to evaluate the expression levels of hsa_circ_0043497 (A) and its top 5 predicted miRNA targets (miR-335-3p, miR-186-5p, miR-380-5p, miR-296-3p and miR-522-3p) (B), hsa_circ_0001204 (C) and its top 5 predicted miRNA targets (miR-612, miR-657, miR-362-3p, miR-377-3p and miR-136-5p) (D) in ten human MDMs after 24 h of infection with H37Rv. [score:5]
For hsa_circ_0001204, the potential miRNAs targets include miR-612, miR-657, miR-362-3p, miR-377-3p and miR-136-5p. [score:3]
[1 to 20 of 2 sentences]
[+] score: 8
In 38 upregulated miRNAs, the fold change in miR-1290 expression in tumor tissues was the highest (17.7-fold), and the expressions of miR-362-5p, -367, -593, -545, -524-5p, -1246, -96, -224, -450a, -7, and -203 were greater than 5-fold (Table S4). [score:8]
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[+] score: 7
Notably, 5 downregulated miRNAs miR-532 and miR-362, miR-500, miR-501, miR-502 are clustered and together encoded in one intron of a renal specific gene voltage-gated chloride ion channel CLCN5, and have been reported to be downregulated in ccRCC [26]. [score:7]
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[+] score: 7
miR-362 was 10 fold more expressed in monocytes and pDCs than in the next highest expressing cell type, T cells. [score:5]
miR-362 and miR-125 were specific to two cells types. [score:1]
A) miR-143 and miR-31 were specific to neutrophils and T cells respectively, while B) miR-362 and miR-125 were specific to monocytes, pDCs and T cells, neutrophils. [score:1]
[1 to 20 of 3 sentences]
[+] score: 6
Other miRNAs from this paper: hsa-mir-122, hsa-mir-155, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-603
Note that more than one miRNAs can share one target site and thus a single SNP can impact the regulation by multiple microRNAs, for example the SNP rs9893667 on gene NM_006380 (APPBP2) can influence the target site of hsa-miR-362-3p, hsa-miR-329, and hsa-miR-603 (highlighted in bold). [score:6]
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[+] score: 6
B. Real-time PCR further revealed that human miR-221-3p, miR-409-5p, miR-1290, miR-155-5p, miR-31-3p, miR-7-5p, miR-362-5p, miR-493-5p, miR-296-5p, and miR-199b-5p were statistically expressed at lower levels in Sertoli cells of SCOS patients than Sertoli cells of OA patients. [score:3]
In contrast, hsa-miR-221-3p, hsa-miR-409-5p, hsa-miR-1290, hsa-miR-155-5p, hsa-miR-31-3p, hsa-miR-7-5p, hsa-miR-362-5p, hsa-miR-493-5p, hsa-miR-296-5p, and hsa-miR-199b-5p were statistically downregulated in human Sertoli cells of SCOS patients compared to OA patients (Figure 3B). [score:3]
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[+] score: 6
Relative expression levels of (B) miR-532-5p, (C) miR-188-3p, (D) miR-362-5p, (E) miR-501-3p, (F) miR-660-3p, and (G) miR-502-5p in triple -negative breast cancer tissues (n = 19) and adjacent normal tissues (n = 4) are shown. [score:3]
miR-532-5p (Figure  2B; mean fold change 2.4), miR-188-3p (Figure  2C; mean fold change 2.5), miR-362-5p (Figure  2D; mean fold change 4.0), miR-501-3p (Figure  2E; mean fold change 5.3), miR-660-3p (Figure  2F; mean fold change 2.2), and miR-502-5p (Figure  2G; mean fold change 3.0) were all markedly up-regulated in the triple -negative breast cancers compared to the normal breast tissue controls. [score:3]
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[+] score: 6
The miRNA expression databases further show that miR-214-3p, miR-212-5p, miR-204-3p, miR-362-3p, miR-450a and miR-320 are expressed in the brain. [score:5]
First, the rs2070736 creates potential binding sites for miR-362-3p and miR-329-3p in the 3′ UTR of DMWD. [score:1]
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[+] score: 5
Interestingly, several of the miRNAs that showed elevated expression in the blood samples of glioblastoma patients (vs healthy control) also exhibited increased expression in glioblastoma stem cells (vs normal neural stem cells) in our study (Table S1), including miR-424, miR-148a, miR-362-3p, miR-30d, miR-128. [score:5]
[1 to 20 of 1 sentences]
[+] score: 4
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-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-495, 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
General increased expression was only observed when HIVE and HIV -positive groups were compared, with miR-19b-2*, miR-937, and miR-362-5p displaying the largest fold changes (213). [score:2]
The combination of six miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-140-5p, and miR-362-3p) generated a biosignature that could distinguish enteroviral patients and HC. [score:1]
Levels of eight circulating serum miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-206, miR-140-5p, miR-455-5p, and miR-362-3p) were significantly higher in sera of patients with enteroviral infections (215). [score:1]
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[+] score: 4
P38 MAPKs (MAPK11, MAPK13, and MAPK14) were found to be regulated by miR-769-5p, miR-146b-5p, let-7g, miR-30b, miR-31, miR-361-3p, and miR-362-3p (Figure 7), which were all down expressed in H1N1 critically ill patients. [score:4]
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[+] score: 4
MiRNAs miR-324-3p (1.73x), miR-1227 (1.95x), miR-362-3p (1.85x), miR-99b-3p (2.21x), miR-19b-1-5p (4.11x), miR-628-3p (2.77x), miR-26a-1-3p (42.47x), miR-576-3p (2.49x) and miR-27a-5p (108x) were up-regulated, in OROV-infected cells relative to uninfected cells. [score:4]
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[+] score: 4
Interestingly, among the miRNAs found to be upregulated in exosomes in response to cytokines, several of them including miR-146a, miR-146b, miR-195, miR-290a-3p, miR-362-3p and miR-497 are known to be involved in cell death [29- 34]. [score:4]
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[+] score: 4
Kang H Downregulation of microRNA-362-3p and microRNA-329 promotes tumor progression in human breast cancerCell. [score:4]
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[+] score: 4
At 6-hour post-infection, miR-126, miR-20a*, miR-362-5p, miR-378, miR-454, and miR574-5p were found to be down-regulated (>2-fold, p<0.05) in H5N1 infected cells. [score:4]
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[+] score: 4
In addition, metformin modulated the expression of a number of miRNAs (let-7f, miR-30b, miR-362, miR-376c, miR-466h, miR-490, and miR-574) involved in the regulation of the cell cycle, which is a crucial mechanism in the AMPK -mediated activity of this drug 42. [score:4]
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[+] score: 4
Other miRNAs approaching significance with log2 fold changes up- or downregulation by greater than 1 included miR-10a, miR-133b, miR-138, miR-150, miR-155, miR-212, miR-362-3p, miR-518e, and miR-885-5p. [score:4]
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[+] score: 3
Christensen L. L. Tobiasen H. Holm A. Schepeler T. Ostenfeld M. S. Thorsen K. Rasmussen M. H. Birkenkamp-Demtroeder K. Sieber O. M. Gibbs P. miRNA-362–3p induces cell cycle arrest through targeting of E2F1, USF2 and PTPN1 and is associated with recurrence of colorectal cancer Int. [score:3]
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[+] score: 3
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-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-130a, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-182, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-10a, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-181a-1, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-138-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-138-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, rno-mir-301a, rno-let-7d, rno-mir-344a-1, mmu-mir-344-1, rno-mir-346, mmu-mir-346, rno-mir-352, hsa-mir-181b-2, mmu-mir-10a, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-125b-1, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-30e, mmu-mir-362, hsa-mir-369, hsa-mir-374a, mmu-mir-181b-2, hsa-mir-346, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-10a, rno-mir-15b, rno-mir-26b, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-34b, rno-mir-34c, rno-mir-34a, rno-mir-106b, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-130a, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-181a-1, hsa-mir-449a, mmu-mir-449a, rno-mir-449a, mmu-mir-463, mmu-mir-466a, hsa-mir-483, hsa-mir-493, hsa-mir-181d, hsa-mir-499a, hsa-mir-504, mmu-mir-483, rno-mir-483, mmu-mir-369, rno-mir-493, rno-mir-369, rno-mir-374, hsa-mir-579, hsa-mir-582, hsa-mir-615, hsa-mir-652, hsa-mir-449b, rno-mir-499, hsa-mir-767, hsa-mir-449c, hsa-mir-762, mmu-mir-301b, mmu-mir-374b, mmu-mir-762, mmu-mir-344d-3, mmu-mir-344d-1, mmu-mir-673, mmu-mir-344d-2, mmu-mir-449c, mmu-mir-692-1, mmu-mir-692-2, mmu-mir-669b, mmu-mir-499, mmu-mir-652, mmu-mir-615, mmu-mir-804, mmu-mir-181d, mmu-mir-879, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-344-2, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-493, mmu-mir-504, mmu-mir-466d, mmu-mir-449b, hsa-mir-374b, hsa-mir-301b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-879, mmu-mir-582, rno-mir-181d, rno-mir-182, rno-mir-301b, rno-mir-463, rno-mir-673, rno-mir-652, mmu-mir-466l, mmu-mir-669k, mmu-mir-466i, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-1193, mmu-mir-767, rno-mir-362, rno-mir-504, rno-mir-582, rno-mir-615, mmu-mir-3080, mmu-mir-466m, mmu-mir-466o, mmu-mir-466c-2, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466p, mmu-mir-466n, mmu-mir-344e, mmu-mir-344b, mmu-mir-344c, mmu-mir-344g, mmu-mir-344f, mmu-mir-374c, mmu-mir-466b-8, hsa-mir-466, hsa-mir-1193, rno-mir-449c, rno-mir-344b-2, rno-mir-466d, rno-mir-344a-2, rno-mir-1193, rno-mir-344b-1, hsa-mir-374c, hsa-mir-499b, mmu-mir-466q, mmu-mir-344h-1, mmu-mir-344h-2, mmu-mir-344i, rno-mir-344i, rno-mir-344g, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-692-3, rno-let-7g, rno-mir-15a, rno-mir-762, mmu-mir-466c-3, rno-mir-29c-2, rno-mir-29b-3, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
1Proliferation, Invasion, Tumor suppression [63– 66] miR-344 ↓2.0 ↓3.2 NA miR-346 ↓2.4Proliferation [67, 68] miR-362 ↓2.3Proliferation, Invasion, Apoptosis [69– 76] miR-369 ↓2.8 ↓2.6 ↓2.1Aerobic glycolysis [77] miR-374 ↑3.0 ↓2.2 NA miR-449 ↑2.7 ↑2.4Proliferation [78– 81] miR-463 ↓2.7 NAmiR-466 [°] ↑2.4 ↑2.1 ↓3.5 NA miR-483 ↓3.2Apoptosis [82] miR-493 ↑2.1 ↓2.2Proliferation [83– 85] miR-499a ↓5.0 ↑2.3Proliferation [86] miR-504 ↓2.6 ↑2.0Proliferation, Apoptosis [87, 88] miR-579 ↑2.8 NAmiR-582 [^] ↑2.4Proliferation [89] miR-615 ↓2.1Proliferation, Invasion [90, 91] miR-652 ↑2.4Proliferation, EMT [92, 93] miR-669b ↓2.1 NA miR-669h ↓3.6 ↑2.3 NA miR-669i ↓2.3 NA miR-669k ↓7.2 ↓5. [score:3]
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[+] score: 3
The rest of co-expressed clusters were listed for regions at 6q13 (including mir-30a and mir-30c-2), Xp11.23 (including mir-362, mir-500, mir-501, mir-502 and mir-532), 14q32.2 (including mir-134, mir-379 and mir-382), 14q32.31 (including mir-127, mir-432 and mir-770), 9q22.32 (including let-7d, mir-23b and mir-27b) and 7q22.1 (including mir-93 and mir-106b) (Table 3). [score:3]
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[+] score: 3
From these 25 miRs, trophoblast cells were found to express 8 at a detectable level: miR-7-5p; miR-186-5p; miR-155-5p; miR-22-3p; miR-185-5p; miR-138-5p; miR-329; and miR-362-3p (Table 1 and Table S1). [score:3]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-17, hsa-mir-28, hsa-mir-223, hsa-mir-127, hsa-mir-188, hsa-mir-194-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-30e, hsa-mir-363, hsa-mir-367, hsa-mir-379, hsa-mir-196b, hsa-mir-450a-1, hsa-mir-431, ssc-mir-28, hsa-mir-493, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-500a, hsa-mir-501, hsa-mir-502, hsa-mir-450a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-506, hsa-mir-508, hsa-mir-509-1, hsa-mir-532, hsa-mir-615, hsa-mir-660, bta-mir-127, bta-mir-30e, bta-mir-17, bta-mir-450a-2, bta-mir-532, bta-mir-363, bta-mir-660, hsa-mir-891a, hsa-mir-892a, hsa-mir-509-2, hsa-mir-450b, hsa-mir-892b, hsa-mir-708, hsa-mir-509-3, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1248, ssc-mir-17, bta-mir-155, bta-mir-188, bta-mir-194-2, bta-mir-196b, bta-mir-223, bta-mir-28, bta-mir-362, bta-mir-367, bta-mir-379, bta-mir-431, bta-mir-493, bta-mir-500, bta-mir-502a-1, bta-mir-502a-2, bta-mir-502b, bta-mir-615, bta-mir-708, bta-mir-1248-1, bta-mir-1248-2, ssc-mir-450a, bta-mir-2320, bta-mir-1388, bta-mir-194-1, bta-mir-450a-1, eca-mir-30e, eca-mir-367, eca-mir-684, eca-mir-196b, eca-mir-615, eca-mir-708, eca-mir-194-1, eca-mir-493a, eca-mir-17, eca-mir-1248, eca-mir-28, eca-mir-127, eca-mir-379, eca-mir-431, eca-mir-493b, eca-mir-155, eca-mir-194-2, eca-mir-188, eca-mir-223, eca-mir-362, eca-mir-363, eca-mir-450a, eca-mir-450b, eca-mir-450c, eca-mir-500-1, eca-mir-500-2, eca-mir-501, eca-mir-502, eca-mir-508, eca-mir-509a, eca-mir-532, eca-mir-660, ssc-mir-30e, ssc-mir-196b-1, ssc-mir-450b, ssc-mir-127, ssc-mir-532, ssc-mir-708, ssc-mir-1285, ssc-mir-500, hsa-mir-514b, ssc-mir-363-1, ssc-mir-450c, hsa-mir-500b, ssc-mir-194b, ssc-mir-155, ssc-mir-362, bta-mir-3601, ssc-mir-615, ssc-mir-2320, bta-mir-450b, ssc-mir-194a, ssc-mir-196b-2, ssc-mir-363-2, ssc-mir-493, hsa-mir-892c, eca-mir-1388, eca-mir-514b, eca-mir-506a, eca-mir-509b, bta-mir-194b, ssc-mir-1388, ssc-mir-223, ssc-mir-660, bta-mir-194b-2, bta-mir-1949
A more difficult case is the mir-532 cluster located on chrX in human (Additional file 1: Figure S14), which contains 8 known miRNAs from miRBase: mir-532, mir-188, mir-500a, mir-362, mir-501, mir-500b, mir-660, mir-502. [score:1]
In pig we found a cluster on chrX of mir-532, mir-188, mir-500, mir-362, mir-500, mir-660, and a mature unknown miRNA picked up by miRDeep. [score:1]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-483
We previously reported that miR-483-3p plays a critical role in the cytotoxic activity of human NK cells [11], and identified miR-362-5p as an essential regulator of NK cell global function via miRNA array analysis [12]. [score:2]
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[+] score: 2
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-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-142, 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-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
More recently, miR-362-5p was found to act as an oncomiR by down -regulating GADD45α, which in turn activated the JNK1/2 and P38 signaling in CML patient samples [45]. [score:2]
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Further analysis revealed that combined six miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-140-5p and miR-362-3p) could discriminate patients with enterovirus infections from healthy controls. [score:1]
In addition, six miRNAs (miR-148a, miR-143, miR-324-3p, miR-628-3p, miR-140-5p and miR-362-3p) possessed the ability to discriminate patients with enterovirus infections from healthy controls [22]. [score:1]
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[27]↓quail myoblasts diff, ↓ C2C12 diff [29] ↓ C2C12 diff [28] ↓ muscle development [32]40miR-320↓(this study)↑ pMyo diff [33]  41 miR-324-3p (n)↑↑(this study)   42 miR-324-5p (n)↑(this study)   43 miR-331 (n)↑(this study)-  44miR-339↓(this study)↑ C2C12 diff [33] ↑ pMyo diff [33]  45miR-361↑(this study)↑ pMyo diff [33]  46 miR-362↑↑(this study)↑ C2C12 diff [28]  47 miR-374 (n)↑(this study)   48 miR-432 (n)↑(this study)   49 miR-451 (n)↓↓↓(this study)   50 miR-452 (n)↓↓(this study)   51 miR-500↑↑(this study)↑ C2C12 diff [28, 33] ↑ pMyo diff [33]  52 miR-501↑↑↑(this study)↑ C2C12 diff [28, 33]  53 miR-502 (n)↑↑(this study)-  54 miR-503↑(this study)↑ C2C12 diff [19, 28, 33] ↑ pMyo diff [33]  55 miR-532↑↑(this study)↑ C2C12 diff [28, 33] ↑ pMyo diff [33]  56↓↓ pMyo diff. [score:2]
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GeneGene-level p-value [a] GS GS p-value MM MM p-valueRank [b] miRNA r [c] p-value FDR GPD1L 2.67E-02 −0.23 1.06E-03 0.90 1.29E-71 1 hsa-miR-210 −0.17 7.37E-03 7.91E-02 CCDC50 2.12E-02 −0.20 4.68E-03 0.85 6.79E-58 2 hsa-miR-501-3p −0.19 3.93E-03 5.05E-02 NAALAD2 8.05E-03 −0.24 5.76E-04 0.85 1.47E-57 3 hsa-miR-140-3p −0.29 1.97E-05 7.98E-04 ALDH1L1 4.94E-03 −0.28 7.13E-05 0.85 3.15E-57 4 hsa-miR-342-5p −0.27 5.13E-05 1. 76E-03 ADH1B 3.14E-02 −0.27 8.82E-05 0.85 4.39E-56 5 — — — — ADH1A 5.00E-02 −0.26 1.83E-04 0.82 2.34E-50 6 hsa-miR-590-3p −0.09 1.06E-01 4.46E-01 PCCA 2.38E-02 −0.21 2.68E-03 0.82 3.87E-49 8 hsa-miR-301b −0.25 2.08E-04 5.42E-03 ORMDL3 3.87E-03 −0.29 3.04E-05 0.80 3.29E-45 9 hsa-miR-362-3p −0.20 2.12E-03 3.23E-02EPB41L4B [d] 7.42E-05 −0.29 3. 47E-05 0.67 2.63E-27 28 has-miR-3613-3p −0.11 6.46E-02 3.4E-01GS, gene significance; MM, module membership. [score:1]
For the hub genes, shown in Table  1, four pairs were identified at FDR < 0.05, including ALDH1L1 and hsa-miR-342-5p (r = −0.27, FDR = 1.76E-03), NAALAD2 and hsa-miR-140-3p (r = −0.29, FDR = 7.98E-04), ORMDL3 and hsa-miR-362-3p (r = −0.20, FDR = 3.23E-02), and PCCA and hsa-miR-301b (r = −0.25, FDR = 5.42E-03). [score:1]
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90 Down 3.84E-18 hsa-miR-4448 2.45 Up 1.66E-04 hsa-miR-1250 −5.71 Down 2.05E-169 hsa-miR-4426 2.23 Up 3.53E-05 hsa-miR-139-5p −5.46 Down 3.71E-25 hsa-miR-720 2.08 Up 1.21E-05 hsa-miR-335-5p −5.26 Down 2.00E-41 hsa-miR-4485 1.71 Up 6.14E-08 hsa-miR-362-3p −5.01 Down 3.36E-10 hsa-miR-877-5p 1.68 Up 1.92E-82 hsa-miR-1255a −4.92 Down 1.25E-62 hsa-miR-3679-5p 1.45 Up 5.53E-04 hsa-miR-3622a-5p −4.83 Down 4.30E-09 hsa-miR-21-3p 1.40 Up 7.87E-13 hsa-miR-1293 −4.67 Down 2.87E-08 hsa-miR-2116-3p −4.64 Down 3.67E-14 hsa-miR-365a-3p −4. [score:1]
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As shown in Figure 4, most transcripts are associated with more than one miRNA, as in the case of TLR4 transcript, correlated with eight different miRNAs (miR-10a-5p, miR-7-5p, miR-135a-3p, miR-103a-3p, miR-7-1-3p, miR-107, miR-629-5p, and miR-362-5p). [score:1]
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It was clearly demonstrated by ROC analysis that the 5-miRNA -based panels (miR-193a-3p, miR-362, miR-572, miR-425-5p, and miR-543) had a high sensitivity and specificity in the discrimination of patients with early-stage RCC from healthy controls [54]. [score:1]
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We analyzed 13 miRNAs that showed significant deregulation in the microarray experiments, including hsa-miR-106b, hsa-miR-107, hsa-miR-1280, hsa-miR-151-3p, hsa-miR-17*, hsa-miR-18a, hsa-miR-199a-5p, hsa-miR-20a, hsa-miR-20b, hsa-miR-30a, hsa-miR-362-3p, hsa-miR-550*, and hsa-miR-664, using TaqMan [® ]MicroRNA Assays (Applied Biosystems). [score:1]
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Seven miRs, including miR-362, -106a, -20b, -363, -542, -450a-1, and -450a-2, were part of a cluster of ≥6 miRs, and miR-485 and -323a were part of a cluster of ≥13 miRs. [score:1]
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healthy controls RT-qPCRSuryawanshi, 2013 [17]miR-362-5p, 1274a, 21, 766, 1975, 1308, 191, 744, 376a, 1246; plasma, EAOC patients vs. [score:1]
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