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17 publications mentioning mmu-mir-491

Open access articles that are associated with the species Mus musculus and mention the gene name mir-491. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 258
miR-491 expression was upregulated in CD8 [+] T cells from colorectal tumour-bearing miceTo investigate the effect of the tumour environment on the expression pattern of miRNAs in the immune system, we conducted a real-time PCR -based high-throughput miRNA array to identify a panel of differentially expressed miRNAs in total CD8 [+] T cells. [score:8]
miR-491 expression was upregulated in CD8 [+] T cells from colorectal tumour-bearing mice. [score:6]
TGF-β1 upregulates miR-491 expression. [score:6]
As expected, miR-491 expression was significantly upregulated (Fig. 6c). [score:6]
Furthermore, we found that miR-491 expression was upregulated by TGF-β1, which is known to limit the activation and function of CD8 [+] T cells. [score:6]
To exclude the possibility that the observed phenotype caused by miR-491 was nonspecific, we overexpressed an irrelevant miRNA, miR-369, with the same retroviral expression vector and transduced CD8 [+] T cells. [score:5]
miR-491 inhibits activated CD8 [+] T cell proliferation and promotes apoptosis by targeting Bcl-xL, CDK4 and TCF1, which results in tumour immune escape. [score:5]
Therefore, the increased sensitivity of miR-491 -overexpressing T cells to AICD may be attributed to the inhibition of the anti-apoptotic molecule Bcl-xL. [score:5]
Therefore, miR-491, which is induced in colorectal tumour-bearing mice, may negatively affect the proliferation of CD8 [+] T cells by targeting CDK4 and TCF-1. Bcl-xL, another identified target of miR-491 in our study, is an anti-apoptotic molecule that belongs to the Bcl-2 family. [score:5]
Bcl-xL, CDK4 and TCF-1 were direct targets of miR-491 in CD8 [+] T cellsTo investigate how miR-491 regulates the proliferation and apoptosis of CD8 [+] T cells, we searched for potential targets of miR-491 using bioinformatics tools (miRecords, http://mirecords. [score:5]
miR-491 overexpression inhibited T cell proliferation. [score:5]
On one hand, the inhibition of miR-491 expression in CTLs may promote their cytotoxic ability and restrict tumour progression. [score:5]
Bcl-xL, CDK4 and TCF-1 were direct targets of miR-491 in CD8 [+] T cells. [score:4]
These results suggest that tcf1and cdk4 are direct targets of miR-491. [score:4]
The results showed that even at about 2-fold upregulation, miR-491 could still limit CD4 [+] and CD8 [+] T cells proliferation and promote apoptosis (Fig. S5). [score:4]
In the tumour animal mo del, miR-491 was upregulated in spleen CD8 [+] T cells from tumour-bearing mice by ~2 fold. [score:4]
To identify the original source of miR-491 upregulation, we further analysed miR-491 level in CD8 [+] T cell subsets between the two groups. [score:4]
miR-491 showed the highest upregulation by 2.2-fold than others (Fig. 1b). [score:4]
TGF-β1 induced miR-491 expression in CD8 [+] T cellsTGF-β plays an important role in regulating immune responses and homeostasis 21. [score:4]
In Jurkat cells, a human T cell line, TGF-β1 caused a 1.81- and 2.81-fold upregulation of miR-491 at 24 hours and 48 hours (Fig. 6b), respectively. [score:4]
Tumour-derived TGF-β induces upregulation of miR-491 in CD8 [+] T cells. [score:4]
To explore whether miR-491 expression was also regulated by tumour cell-derived TGF-β, activated CD8 [+] T cells were co-cultured with diluted MC-38 colorectal cancer cell-conditioned medium (MC-38-CM) for 24 hours. [score:4]
As shown in Fig. 1c, miR-491 was upregulated in effector-like cells (CD44 [high] CD62L [−]) from tumour-bearing mice than controls (P < 0.05). [score:4]
miR-491 overexpression in T cells may compromise the antitumour ability by limiting cell proliferation, promoting cell apoptosis and decreasing IFN-γ production in CD8 [+] T cells. [score:3]
miR-491 inhibits T lymphocyte proliferation. [score:3]
BOSC 23 cells were co -transfected with retroviral expression plasmids, either encoding a miR-491 transcript and CFP or CFP alone (mock), and pCL-Eco retrovirus packaging vector using Lipofectamine LTX and PLUS (Invitrogen). [score:3]
On the other hand, it is necessary to induce miR-491 expression in some tumour cells to perform their antitumour function. [score:3]
To determine whether miR-491 affects T cell survival, apoptosis was induced in miR-491 -overexpressing T cells and mock cells by TCR stimulation. [score:3]
5) (c) CD8 [+] T cell subsets from tumour-bearing mice and controls were sorted by FACS and expression of miR-491 in effector-like, memory and naïve CD8 [+] T cells between the two groups were detected with qPCR (n = 5  vs. [score:3]
The overexpression of miR-491 limited T cell proliferation; the average proliferation rate was 45.4% vs. [score:3]
The results showed that miR-491 overexpression led to enhanced apoptosis in both CD8 [+] and CD4 [+] T cells (Fig. 3a,b). [score:3]
Except for miR-491, TGF-β can alter the expression of numerous miRNAs in CD8 [+] T cells 35. [score:3]
This result indicated that miR-491 could compromise the antitumour ability of CD8 [+] T cells partially through the inhibition of IFN-γ. [score:3]
miR-491 expression was tested at the indicated time by qRT-PCR as described previously. [score:3]
For the apoptosis experiment, miR-491 -overexpressing T cells and mock cells were co-activated by anti-CD3 and anti-CD28 Abs for the indicated time. [score:3]
Then, miR-491 expression was determined by qRT-PCR. [score:3]
These observations suggest that miR-491 could dampen the antitumour ability of effector CD8 [+] T cells by inhibiting IFN-γ production. [score:3]
In breast cancer, miR-491 was identified as an inhibitor of HER2 signalling and induced tumour cell apoptosis 20. [score:3]
miR-491 overexpression facilitated T cell apoptosis. [score:3]
This process resulted in approximately 7- and 5-fold increases in miR-491 expression in CD8 [+] and CD4 [+] T cells, respectively (Fig. 2a,b). [score:3]
Overexpression of miR-491 in CD8 [+] T cells decreased the mRNA levels of bcl2l1, bcl2l2, cdk4, tcf-1 and sh2d2a (Fig. 5a) but only decreased the protein levels of Bcl-xL (encoded by bcl2l1), CDK4, and TCF-1 (Fig. 5b). [score:3]
Thus, we next examined whether TGF-β1 could modulate miR-491 expression in CD8 [+] T cells. [score:3]
Proteins were collected from miR-491 -overexpressing CD8 [+] T cells or mock cells with RIPA buffer (Pierce). [score:3]
TGF-β1 induced miR-491 expression in CD8 [+] T cells. [score:3]
For the analysis of proliferation, miR-491 -overexpressing T cells and mock cells were isolated by density gradient centrifugation and labelled with carboxyfluorescein diacetate succinimidyl diester (CFSE) (5 μM, eBioscience) for 10 minutes at room temperature, and the reaction was stopped with one volume of foetal calf serum. [score:3]
68.47% in miR-491 -overexpressing CD4 [+] T cells and mock cells, respectively (Fig. 2d). [score:3]
76.03% in miR-491 -overexpressing CD8 [+] T cells and mock cells (Fig. 2c), respectively, and 39.77% vs. [score:3]
As shown in Fig. 3c, miR-491 overexpression also enhanced OT-I cell apoptosis. [score:3]
After retrovirus transfection, miR-491 -overexpressing CD8 [+] T cells and mock cells were isolated by flow cytometry. [score:3]
The results showed that miR-369 had no effect on proliferation of CD8 [+] T cells, and the role of miR-491 was not associated with the ectopic expression of vector sequences (Fig. S3). [score:3]
miR-491 acts as a tumour suppressor in several tumours. [score:3]
As shown in Fig. 4b,c, miR-491 -overexpressing CD8 [+] T cells produced substantially less IFN-γ than mock cells. [score:3]
Prediction and validation of miR-491 target genes in CD8 [+] T cells. [score:3]
We separately constructed vectors containing wild-type or mutant miR-491 binding sites in the 3′-untranslated region (3′-UTR) of CDK4 mRNA or TCF-1 mRNA (Fig. 5c). [score:3]
To mimic in vivo condition, we performed miR-491 overexpression by 2.2-fold in CD4 [+] T cells and 2.6-fold in CD8 [+] T cells. [score:3]
Lower expression of miR-491 correlated with poor overall survival of patients with oral squamous cell carcinoma 16. [score:3]
We also discovered that miR-491 -overexpressing CD8 [+] T cells produced less IFN-γ compared with mock cells. [score:2]
miR-491 regulated IFN-γ production in CD8 [+] T cells. [score:2]
Furthermore, miR-491 could apparently regulate T cell proliferation and apoptosis and IFN-γ production. [score:2]
In this study, we determined that tumour-derived TGF-β could induce the expression of miR-491 in CD8 [+] T cells from colorectal tumour-bearing mice compared with their non-malignant counterparts. [score:2]
Mutational 3′-UTRs were constructed by replacing 4 or 5 nucleotides in the miR-491 binding sites with PCR repair. [score:2]
Overall, miR-491 acted as a negative regulator of T cells, especially CD8 [+] T cells, in the tumour environment and may favour tumour immune escape (Fig. 7). [score:2]
These data suggest that miR-491 is regulated by tumour-derived TGF-β in CD8 [+] T cells in a time -dependent manner. [score:2]
Our results indicated that TGF-β produced by tumour cells could modulate miR-491 expression and hence negatively regulate the proliferation and survival of T cells, but it needs further investigation to enclose the mechanism. [score:2]
miR-491 regulates IFN-γ production. [score:2]
To investigate how miR-491 regulates the proliferation and apoptosis of CD8 [+] T cells, we searched for potential targets of miR-491 using bioinformatics tools (miRecords, http://mirecords. [score:2]
miR-491 regulated IFN-γ production in CD8 [+] T cellsIFN-γ is a potent nonspecific tumour cell killer. [score:2]
Notably, in the present study, miR-491 is identified as a negative regulator of T cell function and may contribute to tumour immune evasion. [score:2]
We found that IFN-γ secretion was significantly decreased in miR-491 -overexpressing CD8 [+] T cells compared with mock cells (Fig. 4a). [score:2]
These observations indicate that miR-491 is a positive regulator of T cell apoptosis induced by AICD in vitro. [score:2]
We further examined the role of miR-491 on OT-I cells. [score:1]
These results indicated that miR-491 may be functional in effector like CD8 [+] T cells in tumour microenvironment. [score:1]
To our knowledge, this is the first report to study the role of miR-491 in T cells. [score:1]
Notably, miR-491 has been reported to be induced by TGF-β1 in rat proximal tubular epithelial cells 22. [score:1]
The results showed that TGF-β1 treatment led to a dramatic increase in miR-491 in mouse CD8 [+] T cells by 1.94- and 2.74-fold at 24 hours and 48 hours (Fig. 6a), respectively. [score:1]
Moreover, the induction of miR-491 in CD8 [+] T cells was partially blocked by an anti-TGF-β1 mAb co-cultured with MC-38-CM (Fig. 6d). [score:1]
This evidence suggests that miR-491 may have physiological significance CD8 [+] T cells in vitro even at a relative low level. [score:1]
miR-491 promotes T cell apoptosis. [score:1]
HEK293 cells were seeded in a 96-well plate (1 × 10 [4] per well), and each well was co -transfected with 0.2 μg of wild-type or mutant firefly luciferase reporter vectors, 0.01 μg of pRL-TK (Promega) and miRNA-491 mimics (50 nM) or negative-control scrambled miRNA mimics (50 nM) (RiboBio, China) using Lipofectamine 2000 (Invitrogen). [score:1]
To investigate whether miR-491 affects IFN-γ production, viable miR-491 -overexpressing CD8 [+] T cells were selected and co-activated with anti-CD3 and anti-CD28 Abs for 4 days. [score:1]
However, miR-491 had no effect on mutant vectors (Fig. 5c). [score:1]
Taking together these findings, we show that miR-491 may have a double-edged role in the tumour environment and suggest that alternative manipulation of miR-491 may be required in different cell types during tumour progression. [score:1]
And miR-491 had the tendency for increase in naive cells (CD44 [low] CD62L [+]) and central memory cells (CD44 [high] CD62L [+]) from tumour-bearing mice than controls but the differences did not reach statistical significance. [score:1]
Mo del illustrating the role of miR-491 in CD8 [+] T cells. [score:1]
The role of miR-491 in CD8 [+] T cells during the antitumour immune response is still unknown. [score:1]
To characterize the role of elevated miR-491 in T cells, we constructed a retroviral vector to overexpress miR-491 in T cells. [score:1]
How to cite this article: Yu, T. et al. MicroRNA-491 regulates the proliferation and apoptosis of CD8 [+] T cells. [score:1]
In our study, miR-491 was indeed not abundant in CD8 [+] T cells. [score:1]
We next performed luciferase assays to investigate whether CDK4 and TCF-1 were direct targets of miR-491. [score:1]
The results showed that miR-491 steadily existed in CD8 [+] T cells but was not one of the most highly existed miRNAs (Fig. S1). [score:1]
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2
[+] score: 46
For the other miRNAs, miR-28a-5p, miR-219a-5p, miR-340-5p, and miR-491-5p, which were significantly correlated with the impulsivity trait (Table 3), the expression of three (miR-28a-5p, miR-340-5p, and miR-491-5p) was correlated in the same direction (positive correlation) with the impulsivity trait, whereas the expression of miR-219a-5p was correlated in the opposite direction. [score:7]
Gene products targeted by miR-28a-5p, miR-340-5p, and miR-491-5p are shown in red, a miR-219a-5p target in green, and the miR-340-5p/miR-219a-5p targets in yellow. [score:7]
For the GeneNetwork IDs of individual traits see Table 1. Finally, we established that expression of miR-28a-5p, miR-219a-5p, miR-340-5p, and miR-491-5p, although not directly related to the impulsivity locus or Nrg3, is significantly correlated with the impulsivity trait (Table 3). [score:4]
Based on our results, we propose here that miR219-5p along with miR-340-5p, miR-28a-5p and possibly miR-491-5p could have a key role in the development of psychiatric diseases, possibly by affecting the balance between neuronal outgrowth and differentiation in the context of synapse plasticity, maturation and maintenance. [score:4]
For the GeneNetwork IDs of individual traits see Table 1. Finally, we established that expression of miR-28a-5p, miR-219a-5p, miR-340-5p, and miR-491-5p, although not directly related to the impulsivity locus or Nrg3, is significantly correlated with the impulsivity trait (Table 3). [score:4]
Also, expression of miR-491-5p was weakly positively correlated with these rearing traits. [score:3]
Two mature products of MIR-491 coordinate to suppress key cancer hallmarks in glioblastoma. [score:3]
Three of these miRNAs (miR-28a-5p, miR-340-5p, and miR-491-5p) were negatively correlated with impulsivity, whereas expression of miR-219a-5p showed a positive correlation. [score:3]
Besides miR-190b-5p, the expression of miR-340-5p, miR-28a and miR-491 in the amygdala was negatively correlated with impulsivity. [score:3]
As yet, miR-28a-5p and miR-491-5p have been mainly studied in cancer, and more specifically in the formation of gliomas (Malzkorn et al., 2010; Németh et al., 2013; Li et al., 2014). [score:1]
Contribution of miR-28a-5p, miR-340-5p and miR-491-5p was assessed simultaneously due to their synchronized positive correlation. [score:1]
KEGG biological pathway P-value miR-28a, miR-340, and miR-491 Axon guidance 2.18E-09 Wnt signaling pathway 1.46E-07 Endocytosis 2.38E-07 MAPK signaling pathway 1.28E-05 Focal adhesion 1.40E-05 miR-219a Endocytosis 1.45E-02 Circadian rhythm 2.81E-02 Axon guidance 3.34E-02 Wnt signaling pathway 4.73E-02 Enriched pathways related to neuronal functions are shown. [score:1]
Similarly to the axonal guidance, both of these pathways seem to be more affected by the positively correlated miRNAs (miR-28a-5p, miR-340-5p, and miR-491-5p) rather then the negatively correlated one (miR-219a-5p), of which the effect on these pathways is barely significant (Table 7). [score:1]
Both derivatives of the mir-491 precursor, miR-491-5p and-3p control key hallmarks of glioma carcinogenesis, repressing proliferation (Li et al., 2014; Loos et al., 2014). [score:1]
The effect of miR-219a-5p seems to be small and mainly limited to slits-related guidance cues and (partially) semaphorins cues, whereas the netrins and ephrins cues were affected exclusively by the positively correlated miRNAs (miR-28a-5p, miR-340-5p, and miR-491-5p). [score:1]
The involvement of microRNAs in major depression, suicidal behavior, and related disorders: a focus on miR-185 and miR-491-3p. [score:1]
In addition, in the PFC of depressed patients, as well as in serum of schizophrenic patients, a decrease in miR-491-3p is observed (Cole and Robbins, 1989; Shi et al., 2012; Serafini et al., 2014). [score:1]
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3
[+] score: 41
The expressions of miR-711, miR-714, miR-744, miR-2137, miR-5130, miR-1892, miR-328, miR-346, miR-5099, and miR-705 were significantly upregulated in I/R injured heart grafts, while miR-490, miR-491, miR-210, miR-362, miR-24, miR-423, miR-128, miR-328, miR -181, and miR-532 were downregulated. [score:9]
For example, miR-2137, miR-5130 and miR-5112 were highly expressed in heart tissues; miR-490, miR-491, miR-181, miR-362, miR-425, and miR-3104 were expressed at quite a low level (Ct value ∼ over 30), whereas 32 out of those 58 altered miRNA were expressed at an extremely low level in hearts and there were almost no Ct value detected by qPCR. [score:7]
The findings of our study demonstrate that miR-711, miR-2137 miR-705, miR-5130, miR-346, miR-714, and miR-744 were significantly upregulated (>2 fold change) in I/R injured hearts, while miR-210, miR-490, miR-491, miR-425, miR-423-3p, and miR-532-3p were downregulated. [score:7]
As compared with cells under normxia, miR-711, miR-714, miR-328, miR-346, miR-210, miR-744, miR-5130, miR-181a and miR-2137 were significantly over-expressed in hypoxia/reperfusion treated cardiomyocytes, while the expression of miR-491, miR-211, miR-532, miR-185, miR-425, miR-128, miR-24 was down-regulated (Figure 4B). [score:7]
The expression of miR-491 was slightly but not significantly upregulated in I/R injured grafts. [score:6]
As expected, miR-2137, miR-210, miR-5130, and miR-328 were highly expressed in cardiomyocytes, while miR-490, miR-491, and miR-211 were expressed at a low level. [score:5]
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4
[+] score: 21
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Among the downregulated miRNAs; miR-29 was found to target DNMT1, DNMT3A, DNMT3B and HDAC4),while miR-30 targets DNMT3A, HDAC2, HDAC3, HDAC6 and HDAC10, miR-379 targets DNMT1 and HDAC3 and miR-491 (miR-491 targets DNMT3B and HDAC7. [score:12]
Out of these 25 miRNAs, 18 miRNAs were differentially expressed in a consistent manner between the 2 groups (Figure 4A, highlighted); 8 miRNAs were downregulated in both groups (miR-16, miR-200, miR-205, miR-3064, miR-379, miR-431, miR-485 and miR-491) and 10 miRNAs were upregulated in both groups (miR-194, miR-1894, miR-211, miR-3072, miR- 3077, miR-4436, miR-5128, miR-669a, miR-669c and miR-6967). [score:9]
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5
[+] score: 21
Further, mir-491, a miRNA which is involved in neurosteroidogenesis and pathogenesis of multiple sclerosis [48], was found strongly upregulated by arsenite and downregulated by VPA, and mir-383, a miRNA expressed in the reproductive system and a negative regulator of proliferation, was highly expressed in control samples but significantly downregulated by both substances (4.2- and 2-fold by VPA and arsenite, respectively). [score:15]
In four independent differentiation procedures we could confirm the microarray data (Fig. 5A)–that is, a strong concentration -dependent induction of muscle-specific/abundant miRNA (mir-206, mir-10a, mir-214, mir-145, mir-143, mir-199a) and a significant downregulation of the expression of neuro-specific miRNAs (mir-124, mir-128, mir-137, mir-491, mir-383) in comparison to the solvent control. [score:6]
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6
[+] score: 19
Among these 11 miRNAs, only miR-491-3p was significantly downregulated, while the others were prominently upregulated. [score:7]
miR-2136, let-7f-5p, miR-431-5p, and miR-491-3p were upregulated in both 3-month-old and 6-month-old AD mice, implying their role in the development of AD. [score:5]
Considering a probe signal of over 100 as abundance, eleven of the 28 miRNAs (miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p) were shown to have targets that are tightly related to AD and could easily be detected. [score:3]
Furthermore, levels of miR-2136, let-7f-5p, miR-431-5p, and miR-491-3p were higher in both 3-month-old and 6-month-old APP/PS1 mouse brain, indicating their potential involvement in the progression of AD (Figure 2). [score:1]
miR-491 plays a role in different types of cancers, such as glioblastoma and tongue cancer [40, 41]. [score:1]
To our knowledge, this is the first study to identify the potential effects of miR-342-3p, miR-491-3p, miR-539-3p, miR-376c-3p, miR-10a-5p, and miR-652-5p in the progression of AD. [score:1]
For further analysis, we chose 11 evidently different miRNAs that were conserved between both human and mouse: miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p. [score:1]
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7
[+] score: 18
Of these 15 miRNAs, we selected six miRNAs, miR-451, miR-126, miR-145, miR-146b-5p, miR-491-5p, and miR-107, which were previously reported to have a tumor suppressor role because our previous studies revealed that some tumor suppressor miRNAs in plasma were significantly down-regulated in cancer patients compared with healthy volunteers 30, 32, 33, and the down-regulation of tumor suppressor miRNAs in the blood stream might be related to tumor progression and poor prognostic outcomes [32]. [score:12]
We selected six down-regulated tumor suppressor miRNAs (miR-451, miR-126, miR-145, miR-146b-5p, miR-491-5p, and miR-107) in plasma through a comprehensive miRNA array -based approach. [score:6]
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8
[+] score: 13
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-27b, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-181a-2, mmu-mir-182, mmu-mir-199a-1, mmu-mir-122, mmu-mir-143, mmu-mir-298, mmu-let-7d, 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-15a, mmu-mir-23a, mmu-mir-27a, mmu-mir-31, mmu-mir-98, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-181b-1, mmu-mir-379, mmu-mir-181b-2, mmu-mir-449a, mmu-mir-451a, mmu-mir-466a, mmu-mir-486a, mmu-mir-671, mmu-mir-669a-1, mmu-mir-669b, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-700, mmu-mir-500, mmu-mir-18b, 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-466d, mmu-mir-466l, mmu-mir-669k, mmu-mir-669g, mmu-mir-669d, mmu-mir-466i, mmu-mir-669j, mmu-mir-669f, mmu-mir-669i, mmu-mir-669h, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-466j, mmu-mir-669e, mmu-mir-669l, mmu-mir-669m-1, mmu-mir-669m-2, mmu-mir-669o, mmu-mir-669n, mmu-mir-466m, mmu-mir-669d-2, mmu-mir-466o, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-466c-2, mmu-mir-669a-6, mmu-mir-466b-4, mmu-mir-669a-7, mmu-mir-466b-5, mmu-mir-669p-1, mmu-mir-669a-8, mmu-mir-466b-6, mmu-mir-669a-9, mmu-mir-466b-7, mmu-mir-669p-2, mmu-mir-669a-10, mmu-mir-669a-11, mmu-mir-669a-12, mmu-mir-466p, mmu-mir-466n, mmu-mir-486b, mmu-mir-466b-8, mmu-mir-466q, mmu-mir-145b, mmu-let-7j, mmu-mir-451b, mmu-let-7k, mmu-mir-126b, mmu-mir-466c-3
We also observed downregulated (>1.5-fold) expression of two other miRs: miR-200a and miR-491 in TCDD-exposed fetal thymocytes. [score:6]
Also miR-200a has been shown to regulate apoptosis [83], whereas miR-491 has been shown to induce apoptosis by targeting Bcl-xL gene [40]. [score:4]
miR-200a has been reported to play a crucial role in apoptosis [39], whereas miR-491 has been shown to influence apoptosis by targeting BCL-xL gene in colorectal cancer cells [40]. [score:3]
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9
[+] score: 7
As illustrated in Figure 2, TGF-β1 up-regulates miR-21, miR192, miR-377, miR-382, and miR-491-5p, but down-regulates miR-29 and miR-200 families during renal fibrosis (Kantharidis et al., 2011; Kriegel et al., 2012; Lan and Chung, 2012; Chung et al., 2013a, b). [score:7]
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10
[+] score: 7
A spectrum of miRNAs including miR-337-5p, miR-17-1, miR-15a, miR-491-5p, miR-339, miR-337-3p, miR-241, miR-19a were predicted to down regulate oncogenic targets like TGFβ, BCLXW, BCL-Xl, STATs, c-MYC and SMAD (as represented by red lines). [score:4]
For example, miR-337-5p, miR-17-1, miR-15a, miR-491-5p, miR-339, miR-337-3p, miR-241, miR-19a were found to modulate oncogenic targets including TGFβ, STATs, c-MYC and SMAD. [score:3]
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11
[+] score: 6
Notably, our data revealed that expression of Tnfsf10 (upregulated by ∼2-fold) is likely influenced by several miRNAs including miR-107, miR-145, miR-342-3p, miR-491, miR-494, miR-182, and miR-467a. [score:6]
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12
[+] score: 6
Of the cholinesterase targeting miRNAs, we found 16 that predictably target both BChE and AChE-R, whereas 23 miRNAs show “seed” complementarity to both AChE-R and AChE-S. However, BChE, and the synaptic AChE-S variant share only one single miRNA (Table 1), hsa-miR-491-5p (further details on shared miRNAs can be found in Supplementary Table 2). [score:5]
A functional polymorphism at miR-491-5p binding site in the 3′-UTR of MMP-9 gene confers increased risk for atherosclerotic cerebral infarction in a Chinese population. [score:1]
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13
[+] score: 5
Other miRNAs from this paper: mmu-mir-132, mmu-mir-134
qPCR established that reduced expression of Dgcr8 mRNA in Dgcr8+/-mice at P25 resulted in the reduced expression of a subset of miRNAs (miR-134, 57 ± 6%, P = 0.001; miR-491, 61 ± 6%, P = 0.004; Figure 1C). [score:5]
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14
[+] score: 5
Furthermore, AIV infection leads to the differential expression of cellular miRNA in chickens and mice, and miR491 and miR654 inhibit the replication of H1N1 virus through binding to PB1 in MDCK cells (Song et al., 2010). [score:5]
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15
[+] score: 3
Moreover, several studies have demonstrated that cellular microRNAs (miR-323, miR-491, miR654, miR-146a) inhibit influenza virus replication or propagation [23, 24]. [score:3]
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16
[+] score: 2
Previous studies have demonstrated that several miRNAs are involved in the regulation of HCC angiogenesis, for example, miR-195, miR-491, miR-126-3p, etc [20– 22]. [score:2]
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17
[+] score: 1
The involvement of microRNAs in major depression, suicidal behavior, and related disorders: a focus on miR-185 and miR-491–3p. [score:1]
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