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23 publications mentioning rno-mir-135a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-135a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 50
Of the 123 miRNAs, 15 were differentially expressed in the AS and CS mo del groups, of these, four were significantly upregulated (rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p; Table IV) and 11 were downregulated (significantly downregulated, rno-miR-135a and rno-miR-466b; Table V). [score:12]
Of these 15 miRNAs, rno-miR-296, rno-miR-141, rno-miR-382 and rno-miR-219-5p were significantly upregulated, particularly miR-296 (Table IV), and 11 were downregulated (miR-135a and miR-466b were significantly downregulated, particularly miR-135a; Table V). [score:10]
Sõber et al (21) verified that NR3C2 may be the target gene of miR-135a and is involved in the regulation of blood pressure by inhibiting the in vitro translation of NR3C2 to regulate the angiotensin-aldosterone system balance. [score:9]
In two stress -induced mo dels, rno-miR-296 was the most significantly upregulated and miR-135a was the most significantly downregulated. [score:7]
We hypothesized that miR-135a may interact with the target genes to inhibit sympathetic nerve excitation and suppress the HPA axis and the renin-vascular angiotensin system, resulting in the release of a variety of stress hormones, including catecholamines, cortical hormone, pancreatic glucagon and renin, thus protecting the myocardium from injury. [score:7]
In the present study, miR-135a was significantly downregulated. [score:4]
In conclusion, rno-miR-296, rno-miR-141, rno-miR-382, rno-miR-219-5p, miR-135a and miR-466b may be involved in stress at the molecular level, thus causing myocardial injury. [score:1]
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2
[+] score: 44
RDX could first up-regulate the expression of miR-71, miR-27ab, miR-98, and miR-135a, then reduce the expression of the gens POLE4, C5ORF13, SULF1 and ROCK2, and eventually induce neurotoxicity. [score:8]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGFBiological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
MiRNAs Target Genes Names Regulation Up Down miR-135a Up KIAA1033, CEP350, ROCK2 miR-320 Down BANP, CALD1, POLE4 miR-98 Up SULF1 miR-129* Down BANP, FAM82A2 miR-27ab Up HMGCR, LITAF, NPTX2 CALD1, C5orf13, KIAA1033 miR-342-3P Down VGF KIAA1033 miR-7a Up SLC38A2 POLE4, SLC35E4, C5orf13 miR-674-5p Up VGF Biological functional analysis revealed that more than half (8) of the overlapped genes are involved in neurological diseases and nervous system function (Table 4). [score:6]
The induction of miR-71, miR-27ab, miR-98, and miR-135a expression by RDX, could reduce the expression of the genes POLE4, C5ORF13, SULF1 and ROCK2, and eventually induce neurotoxicity. [score:5]
RDX could first induce the expression of miR-71, miR-27ab, miR-98, and miR-135a, then reduce the expression of POLE4, C5ORF13, SULF1 and ROCK2, and finally induce neurotoxicity. [score:5]
RDX could first induce the expression of miR-71, miR-27ab, miR-98, and miR-135a, then reduce the expression of POLE4, C5ORF13, SULF1 and ROCK2, and finally induce neurotoxicity, which provides an alternative mechanism to explain RDX induced neurotoxicity. [score:5]
As shown in table 3 the targets of miR-135a, miR-98, and most of the targets of miR-7a have an inverse relationship with their responsive miRNAs. [score:5]
Of these 9 miRNAs, 6 miRNAs including miR-98, miR-27b, miR135a, miR-7a, miR-674-5p and miR-27a were significantly up-regulated by RDX. [score:4]
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3
[+] score: 38
Interestingly, PNM overexpression in B13 cells upregulated the expression of miR-137-3p, miR-135a-5p and miR-204-5p and repressed the expression of miR-210-3p to the same levels of those detected in rat islets, highlighting the potential role of these miRNAs in the reprogramming process. [score:10]
B13 cells that were transduced with Ad-PNM showed upregulation of 6 miRNAs (miR-134-5p, miR-455-3p, miR-384-5p, miR-137-3p, miR-135a-5p and miR-22-5p) and downregulation of 2 miRNAs (miR-335-3p and miR-148a-5p). [score:7]
The up-regulation of miR-455-3p, miR-137-3p and miR-135a-5p due to PNM expression observed in our panels (Table 3) was also validated in this single PCR study (Fig 6H–6J). [score:6]
Furthermore, expression levels of miR-137-3p, miR-135a-5p, miR-204-5p, miR-210-3p in reprogrammed B13 cells were consistent with the expression levels detected in rat islets and markedly differed from those displayed by rat exocrine tissue. [score:5]
To the best of our knowledge, there are no reports describing a link between β cell development or function and the remaining overexpressed miRNAs that were identified in the present study: miR-455-3p, miR-384-5p, miR-137-3p and miR-135a-5p. [score:4]
Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
0145116.g006 Fig 6Relative miRNA expression levels of miR-200c-3p (A), miR-141-3p (B), miR-325-3p (C), miR-2137 (D), miR-210-3p (E), miR-181a-5p (F), miR-204-5p (G), miR-455-3p (H), miR-137-3p (I), miR-135a-5p (J), miR-384-5p (K) in rat exocrine fractions, rat islets, AR42J cells, B13 cells and B13 transduced with Ad-GFP or Ad-PNM at 4 days post-transduction, quantified by individual qPCR assays. [score:2]
Of note, using single qPCR assays we demonstrated that miR-455-3p, miR-137-3p and miR-135a-5p were expressed at very similar levels in reprogrammed B13 cells and pancreatic islets, suggesting a mechanistic relationship between these miRNAs and insulin production and/or β cell phenotype. [score:2]
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4
[+] score: 20
Our results showed that anhedonic animals exhibited decreased expression of two miRNAs potentially involved in negative regulation of SERT (miR-18a-5p and miR-135a-5p) in PCx as compared to non-stressed animals. [score:3]
In our study, we observed an interesting relationship: Decrease in miRNA expression in PCx of stressed animals was accompanied by an increase in miRNA expression in VTA; however, it should be noted that we observed a lack of effect of miR-135a-5p in VTA, and this observation needs further investigation. [score:3]
The Effect of 2 Weeks of CMS on the Expression Levels of miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, and miR-872-5p in Mesocortical Pathway. [score:3]
Moreover, statistical analysis showed that stress exposure for two consecutive weeks also decreased the expression levels of all examined miRNAs (except miR-34a-5p, see Fig. 3b) in rat PCx (Fig. 3a, c–f) as compared to control group of rats (miR-18a-5p F [2,29] = 14.19, p < 0.0001; miR-135a-5p F [2,29] = 16.95, p < 0.0001; miR-195-5p F [2,29] = 4.13, p < 0.02; miR-320-3p F [2,29] = 10.57, p < 0.001; miR-674-3p F [2,29] = 4.03, p < 0.05; miR-872-5p F [2,29] = 15.67, p < 0001). [score:2]
One-way ANOVA revealed increased expression levels of all miRNAs of interest (except miR-135a-5p, see Fig. 3c) after 2 weeks of CMS in VTA (Fig. 4a, b, d–g) of stressed animals as compared to non-stressed group of rats (miR-18a-5p F [2,29] = 4.34, p < 0.05; miR-34a-5p F [2,29] = 8.03, p < 0.01; miR-195-5p F [2,29] = 12.88, p < 0.001; miR-320-3p F [2,29] = 11.31, p < 0.001; miR-674-3p F [2,29] = 19.99, p < 0.0001; miR-872-5p F [2,29] = 18.18, p < 0.0001). [score:2]
Dynamic Changes in the Serum Levels of miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, and miR-872-5p during 2 Weeks of the CMS Procedure. [score:1]
Based on our previous study [20] and literature survey, we chose a set of seven different miRNAs (i. e., miR-18a-5p, miR-34a-5p, miR-135a-5p, miR-195-5p, miR-320-3p, miR-674-3p, miR-872-5p) which are associated with stress response and functioning of the central nervous system. [score:1]
Issler et al. have shown that miR-135a has been associated with stress resilience and antidepressant treatment. [score:1]
miR-135a-5p was not detectable in rat serum. [score:1]
miR-135a-5p has been shown to mediate anxiety-like and depression-like behaviors as well as antidepressant response [13]. [score:1]
Serum level of miR-135a-5p was undetectable. [score:1]
The authors even postulate that miR-135a may act as an endogenous antidepressant [13]. [score:1]
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5
[+] score: 19
MiR-21, miR-31 and miR-488 are down-regulated, while miR-153, miR-135b, miR-135a and miR-298 are up-regulated in secretory-stage enamel formation compared to maturation-stage. [score:6]
In contrast, as seen in the in situ slides, there was a decrease in the expression levels of miR-153, miR-135b, miR-135a and miR-298 from secretory-stage to maturation-stage tooth development (Figure  6K-R). [score:4]
The expression patterns of seven selected miRNAs (miR-21, miR-31, miR-488, miR-153, miR-135b, miR-135a and miR-298) were examined (Figure  6E-R). [score:3]
Seven differentially expressed miRNAs (miR-21, miR-31, miR-488, miR-153, miR-135b, miR-135a and miR298) in secretory- and/or maturation-stage enamel organs were confirmed by in situ hybridization. [score:3]
This trend of expression correlates well with the miRNA qPCR array data (i. e., miR-153, miR-135b, miR-135a and miR-298 changed by -3.7, -12.4, -8.9 and -4.3 fold, respectively) (Additional file 1). [score:3]
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6
[+] score: 19
We selected up-regulation of oncogenic miRNAs such as mir-21 as well as down-regulation of the tumor suppressor miRNAs Let-7e, mir-135a, and mir-375 for our analysis. [score:9]
In patients, miR-135a inhibits cancer cell proliferation and exhibits the properties of a tumor suppressor in renal-cell carcinoma [39], while its target oncoprotein BAG-1 increases more than 4 fold as determined by proteomics. [score:7]
Moreover, the oncogenic miRNA, mir-21 was increased 3.8 fold, whereas the tumor suppressor miRNAs, Let-7e, mir-135a, and mir-375 were decreased by 2.9, 2.7 and 5.9 fold, respectively. [score:3]
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7
[+] score: 10
Among the other novel predictions, (miR-135a, -203, -335, -338-3p and -93), miR-335 that has two binding sites on the 3'UTR of Hif-1a was found to be the most promising regulator of Hif-1a expression (Fig 2). [score:4]
Among the 10 miRNAs, interaction of miR-17, -18a, -20a and -20b-5p with HIF-1a had been reported previously in cancer pathogenesis [16, 22] whereas the remaining six miRNAs, miR-135a/b, -203, -335, -338-3p and -93 had not been validated in any disease condition. [score:3]
miR-135a, -203 and -338-3p did not show direct interaction with Hif-1α (Fig 2B). [score:2]
As miR-135a and miR-135b only differs by one nucleotide in a non-seed region, miR-135a was selected for validation studies. [score:1]
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8
[+] score: 10
Male-biased miRNA expression was observed for miR-206 and miR-135a (Figure  5D-E), both of which showed higher expression in males at 21 weeks of age. [score:5]
Male-biased miRNA expression was associated with pathways related to cancer (miR-130b, miR-214, miR-181b, miR-199a, miR-150, miR-135a, miR-142-3p, miR-142-5p, miR-185), hematological disease (miR-22*, miR-142-3p, miR-142-5p, miR-150, miR-181b), and renal inflammation/nephritis (miR-130b, miR-223, miR-150, miR-142-5p, miR-296*, miR-185-3p) (Additional file 2). [score:5]
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9
[+] score: 9
To confirm findings from miRNA array study, five miRNAs (miR-129, miR-135a, miR-191, miRNA-22 and miR-26b) were chosen to examine their expression in rat hippocampus by quantitative RT-PCR (qRT-PCR). [score:3]
As shown in Figure  2, levels of miR-129, miR-135a and miRNA-22 were significantly up-regulated in hippocampus in CCE rats, as compared to that in SCE rats (p < 0.05). [score:3]
Twelve miRNAs (miR-135a, miR-190, miR-22, miR-347, miR-376*, miR-380*, miR-382, miR-383, miR-702-3p, miR-708, miR-873, and miR-99b*) were regulated only in CCE rats (p < 0.05 vs. [score:2]
Notably, some miRNAs levels selectively affected in CCE rats, but not in CCA rats, such as miR-129, miR-135a and miR-22 in this study. [score:1]
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10
[+] score: 9
As shown in Figure 1E, F, miR-153 expression was elevated and miR-222 expression was decreased at 24 hours post-CCI; expression of both miR-135a and miR-135b was reduced at 7 days post-CCI; miR-124 expression was comparable in control and CCI samples at both the 24-hour and 7-day time points. [score:9]
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11
[+] score: 5
Notably, a panel of 11 Runx2 -targeting miRNAs (miR-23a, miR-30c, miR-34c, miR-133a, miR-135a, miR-137, miR-204, miR-205, miR-217, miR-218, and miR-338) is expressed in a lineage-related pattern in mesenchymal cell types [20]. [score:5]
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12
[+] score: 5
Targeting of Runx2 by miR-135 and miR-203 impairs progression of breast cancer and metastatic bone disease. [score:5]
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13
[+] score: 5
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-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, 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-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, 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-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
Cesana et al. showed that a long-intergenic ncRNA (lincRNA), linc-MD1, regulates muscle differentiation by interacting with two miRNAs, miR-135 and miR-133, which can bind to MAML1 and MEF2C to regulate their expression levels. [score:5]
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14
[+] 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-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, 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-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-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, 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-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The prospect that a similar function may extend to other miRNAs is suggested by the conservation of several miRNAs (e. g. miR-25, miR-34a/b/c, miR-135a/b, miR-194, and miR-200a) that are capable of directly targeting the Wnt/β-catenin, a signaling pathway that has been wi dely implicated in the control of oncogenic hallmarks such as cell proliferation, metastasis, angiogenesis, telomerase activity, and apoptosis (reviewed by [49]). [score:4]
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[+] score: 4
For instance, recent reports have indicated that both APC and MMR gene expression is regulated by miRs (e. g. miR-135 and miR-155, respectively) [10], [16]. [score:4]
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16
[+] score: 3
However, there were striking differences in the expression of miRNAs such as miR-135a, miR-429, miR-200a/b and miR-215 which were not detected in our samples but were reported to be significantly decreased by Zhao et al [38]. [score:3]
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[+] score: 3
Zhu et al. has recently demonstrated that increased expression of miR-135a, protects diabetic mice against ischemia/reperfusion injury [58]. [score:3]
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[+] score: 3
In addition, overexpression of miR-135a in 5HT Neurons was proved to reduce depression-like behaviors (Heyer and Kenny, 2014; Issler et al., 2014). [score:3]
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[+] score: 2
Linc-MD1 is required for appropriate muscle differentiation, at least in part because it regulates the levels of myocyte enhancer factor 2C (MEF2C) and mastermind-like protein 1 (MAML1) by sponging endogenous miR-133 and miR-135 in the cytoplasm of muscle cells [24]. [score:2]
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20
[+] score: 2
For example, miR-218, miR-324-5p, miR-365 and miR-146a were localized on chromosome 10; miR-764-5p and miR-351 on chromosome X; miR-101 and miR-30e on chromosome 5; miR-582 and miR-137 on chromosome 2; miR-153 and miR-203 on chromosome 6; miR-124 and 181a on chromosome 3 and miR-135a*/miR-135a-3p and let-7i on chromosome 7. Some of the miRNAs that were localized on the chromosome and in close proximity showed the same direction of changes. [score:2]
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[+] score: 2
According to our in silico analysis, Ppar γ is likely regulated by microRNAs like let-7 family members, miR-30 family members, miR-27b, miR-23ab, miR-93, miR-25, miR-128ab, miR-320, and miR-135. [score:2]
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[+] score: 2
The lncRNA linc-MD1 competes with miR-133 and miR-135 to regulate myoblast differentiation [55]. [score:2]
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[+] score: 1
As seen in the kidneys, two miRNAs, namely miR-135 and miR-199a-5p remained unaltered. [score:1]
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