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24 publications mentioning mmu-mir-495

Open access articles that are associated with the species Mus musculus 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.

1
[+] score: 160
By interfering with miR-495 and its target gene PHLPP in xenograft tumors in nude mice, we found that upregulating miR-495 expression or inhibiting PHLPP expression could increase phosphorylated AKT and phosphorylated Survivin levels, leading to inhibited apoptosis and enhanced growth of GBC xenograft tumors. [score:14]
Further, downregulation of miR-495 expression or increased PHLPP expression was able to reduce the level of phosphorylated AKT and phosphorylated Survivin, leading to the induction of apoptosis and inhibited tumor growth. [score:10]
Increasing the expression of miR-495 in GBC cells enhanced cell proliferation, and inhibition of miR-495 expression in GBC cells decreased cell viability. [score:7]
Inhibiting the expression of miR-495 in GBC cells led to an increase of PHLPP expression. [score:7]
After the intervention therapy, within 14 days, tumors in the Ad5-PHLPP treatment group showed significant growth inhibition compared with the control group; within 21 days, tumors in the miR-495 inhibitor group showed growth inhibition, whereas tumors in the Ad5-shPHLPP group and the miR-495 mimic group had accelerated growth (Fig. 6A). [score:6]
Many tumor tissues, including GBC, show high expression of miR-495 and low expression of PHLPP. [score:5]
After confirming miR-495 expression levels, the PHLPP expression was detected by Western blot, with GAPDH as the loading control. [score:5]
Gene therapy intervention specific for miR-495 and its target gene PHLPP may provide an effective alternative strategy to develop target therapies for GBC. [score:5]
Mice in the miR-495 mimic and miR-495 inhibitor groups received injections of miR-495 mimic and miR-495 inhibitor (Guangzhou RiboBio Co. [score:5]
Using miRNA target gene prediction software (miRanda, TargetScan, picTar), we found that the 3′-UTR of PHLPP contains a seed sequence that combines miR-495 (GTTTGTT). [score:5]
The reduced expression of PHLPP in GBC cells is associated with high expression of miR-495. [score:5]
This study reveals the role and mechanism of PHLPP and Survivin in GBC cells and proposes strategies for gene therapies targeting the miR-495/PHLPP/AKT/Survivin regulatory pathway, which have important application prospects in the comprehensive treatment of GBC. [score:4]
Compared the cell proliferation activities of miR-495 mimic -transfected cells and miR-495 inhibitor -transfected cells, we found that the viability of miR-495 mimic -transfected cells was significantly higher than that of miR-495 inhibitor -transfected cells both at 48 h and 72 h after transfection (Fig. 5D). [score:4]
We hypothesize that PHLPP may be a potential target of miR-495. [score:3]
Fresh tissues from 30 cases of primary tumor tissue GBC, 10 cases of liver metastasis GBC tissues and 10 cases of normal gallbladder mucosa tissues were preserved for detecting miR-495 expression levels by qRT-PCR. [score:3]
We found that miR-495 expression was significantly higher in GBC tissues than in normal tissues, and was higher in GBC metastatic tissues than in primary tumors (Fig. 5A). [score:3]
Compare with the control group, the weights of the tumors in the Ad5-PHLPP group and in the miR-495 inhibitor group were significantly lower, and the weights of the tumors in the Ad5-shPHLPP group and in the miR-495 mimic group were significantly higher (Fig. 6B). [score:3]
In tumors of the miR-495 inhibitor group, the p-AKT and p-Survivin levels were decreased, and the apoptosis rate was increased. [score:3]
Using qRT-PCR, we detected the miR-495 expression level in 30 cases of GBC primary tumor tissues, 10 cases of GBC liver metastatic tissues and 10 cases of normal gallbladder mucosa tissues. [score:3]
Decreased PHLPP levels was associated with high miR-495 expression in GBC cells. [score:3]
High expression of miR-495 in GBC tumor cells may be a major mechanism of PHLPP inactivation, cell resistance to apoptosis and enhanced proliferation. [score:3]
Next, 1 × 10 [6] EH-GB1 and GBC-SD cells were seeded in 24-well plates and transfected with miR-495 mimic or miR-495 inhibitor at 20 μg / well using Lipofectamine [TM] 2000 (Invitrogen, Carlsbad, CA). [score:3]
The remaining 25 animals were randomly divided into five groups (Ad5-PHLPP, Ad5-shPHLPP, miR-495 mimic, miR-495 inhibitor, and blank control groups). [score:3]
These results suggested that PHLPP is a target gene of miR-495. [score:3]
In contrast, cells transfected with miR-495 inhibitor had an increased luciferase activity (Fig. 5C). [score:3]
Therefore, we hypothesized that PHLPP is a potential target of miR-495. [score:3]
Figure 5(A) The expression of miR-495 in 30 cases of GBC primary tumor tissues, 10 cases of GBC liver metastatic tissues and 10 cases of normal gallbladder mucosa tissues was examined by qRT-PCR. [score:3]
miR-495 expression in GBC tissues and cell lines. [score:3]
EH-GB1 and GBC-SD cells at 1 × 10 [6] cells/well in 24-well plates were transfected with miR-495 mimic or miR-495 inhibitor at 20 μg/well and cultured for 24 h. The wells were co -transfected with 20 ng pRL-TK together with 200 ng pGL3-miR495Luc, pGL3-miR495Ctrl, or pGL3-Control. [score:3]
Each mouse received a total dose of 1 × 10 [9] pfu adenovirus, or 50 μg miR-495 mimic and miR-495 inhibitor. [score:3]
The miR-495 expression was determined using the MiniOpticonTM Two-Color Real-Time PCR Detection System (Bio-Rad, Hercules, CA, USA), with U6 as an internal reference. [score:3]
High expression of miR-495 in GBC cells may be a major mechanism of PHLPP inactivation and increased proliferation of cancer cells. [score:3]
Treatment of cells with miR-495 inhibitor resulted in increased PHLPP levels (Fig. 5B). [score:3]
PHLPP was regulated by miR-495 in GBC cells. [score:2]
However, PHLPP, that is under the regulation of miR-495, may dephosphorylate AKT and inactivate AKT signaling pathway, and also possibly dephosphorylate Survivin and promotes Survivin transportation into nuclei, then inactivates the function of Survivin, finally results in an increase of cell apoptosis and decrease of cell proliferation. [score:2]
The results suggested that miR-495 is exactly an upstream regulator of PHLPP. [score:2]
In summary, our experiments showed that a miR-495 / PHLPP / AKT / Survivin pathway regulates the conversion between apoptosis and proliferation of GBC cells (Fig. 7). [score:2]
The schematic diagram of miR-495/PHLPP/AKT/Survivin regulatory pathway potentially existed in GBC. [score:2]
With EH-GB1 xenograft mo del in nude mice, we studied the effects of interfering with the miR-495/PPHLP1/AKT/Survivin pathway on GBC xenograft tumors. [score:1]
Effect of PHLPP or miR-495 on mouse GBC xenograft mo del. [score:1]
The PHLPP 3′-UTR contains a seed sequence that combines miR-495. [score:1]
By mutating the complement sequences of the miR495 seed sequence in PHLPP 3′-UTR, we constructed a negative control vector pGL3-miR495Ctrl in which the miR-495 binding sites were mutated. [score:1]
After transfected with miR-495 mimic in EH-GB1 and GBC-SD cells, the luciferase activity was decreased. [score:1]
The miR-495 levels were high in both EH-GB1 and GBC-SD cells. [score:1]
Once the tumors were formed, experiments interfering with PHLPP and miR-495 were performed. [score:1]
Luciferase reporter gene assay confirmed that miR-495 plays a regulatory role by binding to the PHLPP 3′-UTR. [score:1]
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2
[+] score: 24
We conclude that miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543 represent an FGF2 -dependent system of multiple miRNAs that target specific genes operating in pathways and processes related to the lens differentiation (via c-Maf, Med1/PBP, N-myc, and Nfat5), miRNA-regulated RNA processing (via Cpsf6 and Tnrc6b) and nuclear/chromatin -based processes (via Med1/PBP, As1l, and Kdm5b/Jarid1b/Plu1). [score:4]
Three miRNAs from this cluster, including miR-495, miR-543, and miR-381, represent a group of most highly connected miRNAs in this system (Figure 6A) and regulate together multiple genes known to regulate lens fiber cell differentiation, including c-Maf (Figure 7 and Figure 10). [score:3]
The total number of their target genes is between 114 (1st rank, “early” miR-495) and 45 (10th rank, “early” miR-31 and miR-133b) connections. [score:3]
We found that seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, target at least two “early” genes examined (i. e., c-Maf, N-Myc, and Nfib). [score:3]
We predict that several important regulatory genes of lens fiber cell differentiation, including c-Maf, Kdm5b/Jarid1b, Med1/PBP, Nfat5/OREBP, and N-Myc, are connected by multiple shared miRNAs, with four of them, including miR-381, miR-495, miR-382, and miR-543, encoded by a miRNA cluster on rat chromosome 6, a syntenic region with mouse chromosome 12, and human 14q32.2 imprinted regions. [score:2]
This gross analysis is consistent with our findings of genes regulated by miR-495, miR-543, and miR-381 in lens that belong to these similar categories (Figure 5). [score:2]
Both c-Maf and Med1/PBP are predicted to be regulated by similar miRNAs, including miR-137, miR-200c, and miR-495 (Figure 7). [score:2]
The most connected miRNA identified here through the 12 top-ranking transcripts, including miR-495, miR-200c, miR-543, miR-381, and miR-9 (Figure 6A), retained their high-connectivity positions as identified by independent analysis shown earlier in Figure 6A. [score:1]
The miR-495 and miR-543 are neighbors, and miR-381 is located ~12.7 kb from miR-495. [score:1]
Seven miRNAs, including miR-9, miR-137, miR-200c, miR-381, miR-455, miR-495, and miR-543, and connections to specific functional groups of genes are shown. [score:1]
The miR-381, miR-495, miR-543, and miR-382 form a miRNA-gene cluster on rat chromosome 6q32. [score:1]
Notably, miR-381, miR-495, and miR-543 form a miRNA-gene cluster on rat chromosome 6, and its syntenic regions on mouse and human chromosome 12 and 14, respectively (Sewer et al. 2005). [score:1]
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3
[+] score: 17
It is important to note that only 9 miRNAs (miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p) were significantly upregulated or downregulated in both lungs infected with either wild type w81 or the mouse-adapted ma81 strain at all time points (Tables  1 and 2). [score:7]
Twenty-seven and 20 differentially expressed miRNAs identified to be commonly presented at 1 and 3 dpi were presented in Tables  3 and 4. Of these, only miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p were commonly upregulated at both 1 and 3 dpi. [score:6]
It is noteworthy that only 9 miRNAs (miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p) were significantly upregulated in both lungs infected with either wild type w81 or the mouse-adapted ma81 strain at both time points. [score:4]
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4
[+] 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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5
[+] score: 9
The first, Pten, was upregulated (1.38-fold change and P=2.5E–03) and the three miRNAs (mir-369-5p, mir-25 and mir-495) predicted to target it were downregulated, with mir-369-5p belonging to the Dlk1-Dio3 cluster (Fig. 7). [score:9]
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6
[+] 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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7
[+] score: 8
Other miRNAs from this paper: mmu-mir-154, mmu-mir-299a, mmu-mir-299b
Expression of miR-495 and miR-299-5p, both localized to the chromosome 14q32 cluster, were also upregulated in a setting of MI and inversely correlated to cardiac function (Supplementary Fig. S5B,C) 4. Thus, further improvements in cardiac function and pathology may be observed if multiple members of the 14q32 cluster are inhibited. [score:8]
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8
[+] score: 7
Number of target genes predicted for each differentially expressed miRNA varied from 12 (miR-676) to 826 (miR-495), with an average of 190 for miRNAs overexpressed in FCx and 132 in HP (Figure 4). [score:7]
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9
[+] 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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10
[+] 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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11
[+] score: 5
Other miRNAs from this paper: mmu-mir-150, mmu-mir-22, mmu-mir-196b
Jiang X MiR-495 is a tumor-suppressor microRNA down-regulated in MLL-rearranged leukemiaProc. [score:5]
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12
[+] score: 4
Impressively, of the 17 upregulated miRNAs in MRL- lpr mice, 11 miRNAs (miR-154, miR-127, miR-379, miR-382, miR-433, miR-300, miR-376b, miR-394, miR-299, miR-495, and miR-329) are located at a genomic imprinted DLK1-Dio3 region. [score:4]
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13
[+] score: 3
Other miRNAs from this paper: hsa-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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14
[+] score: 3
Inhibition of 14q32 microRNAs miR-329, miR-487b, miR-494 and miR-495 increases neovascularization and blood flow recovery after ischemia. [score:3]
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15
[+] score: 3
For instance, high expression levels of miR-98-5p, miR-302e, miR-495-3p, and miR-613 are significantly correlated with the radiosensitivity of NSCLC patients [10]. [score:3]
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16
[+] score: 3
Other miRNAs from this paper: mmu-mir-144, mmu-mir-486a, mmu-mir-486b
This approach confirmed the differential expression of several miRNAs such as miR-495 and miR-486, which are involved in cancer cell growth and invasion in vitro and in vivo [30, 31]. [score:3]
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17
[+] score: 3
Welten S. M. Bastiaansen A. J. de Jong R. C. de Vries M. R. Peters E. A. Boonstra M. C. Sheikh S. P. La Monica N. Kandimalla E. R. Quax P. H. Inhibition of 14q32 microRNAs miR-329, miR-487b, miR-494, and miR-495 increases neovascularization and blood flow recovery after ischemia Circ. [score:3]
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18
[+] score: 3
Welten SM 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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19
[+] 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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20
[+] 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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21
[+] score: 1
More than 40 microRNAs in the Uup group were shared by the above pathways, while miR-503, miR-122, miR-495, and miR-382 were exclusively involved in the focal adhesion pathway, and miR-150, miR-411, miR-146a/b exclusively participated in the MAPK pathway (S4 Table). [score:1]
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22
[+] 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-495, 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-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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23
[+] score: 1
Formosa A. Markert E. K. Lena A. M. Italiano D. Finazzi-Agro E. Levine A. J. Bernardini S. Garabadgiu A. V. Melino G. Candi E. MicroRNAs, 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. [score:1]
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24
[+] score: 1
S7 7. Nrf2 -dependent effect of 5 mg / kg PQ Nrf2(+/+) PQ5—Nrf2(–/–) PQ5 miR-135a, miR-376c, miR-31, miR-let-7i*, miR-669b*, miR-344, miR-15b, miR-700*, miR-3099, miR-377, miR-338-5p, miR-382, miR-219-3p and miR-310a S8 8. Nrf2 -dependent effect of 10 mg / kg PQ Nrf2(+/+) PQ10—Nrf2(–/–) PQ10 miR-495*, miR-154*, miR-let-7b, miR-1983, miR-103 and miR-26a S9 The miR-380-3p / Sp3 mRNA pathway is worth to mention here. [score:1]
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