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13 publications mentioning rno-mir-381

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-381. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 216
Other miRNAs from this paper: rno-mir-183, rno-mir-200b, rno-mir-182
Ectopic LRRC4 overexpression in U251 cells (Figure 5D) and 5-Aza-dC -mediated re -expression of LRRC4 in U251, SF126, and SF767 cells (Figure 5E) led to suppression of BRD7 expression, suggesting that miR-182 and miR-381 silencing inhibited BRD7 expression by targeting LRRC4. [score:15]
We have confirmed that LRRC4 is a target gene of miR-381, at the same time, overexpression of LRRC4 also downregulated the expression of miR-381 in glioma cells, the interaction of miR-381 and LRRC4 is involved in glioma growth [17]; when the miRNAs were used for query, it was found that miR-381 targets both LRRC4 and BRD7, which is cloned by our laboratory [18]. [score:12]
BRD7 isn’t the target gene of miR-381, but miR-381 did downregulated the expression of BRD7. [score:8]
However, overexpression of miR-381 mimics did downregulated the expression of BRD7 (Figure S1). [score:8]
Thus, it was suggested that LNA -mediated miR-182 and miR-381 silencing down-regulated the expression of BRD7 by restoring LRRC4 expression in gliomas. [score:8]
These results suggested that miR-182 and miR-381 silencing modulated the ERK/MAPK and PI-3K/AKT signaling pathways, thereby inhibiting the expression of AP2, SP1, and E2F6 and promoting c-Myc expression. [score:7]
Suppressing endogenous expression of miR-182 and miR-381, respectively, restored the activation of LRRC4 in gliomas, and inhibited glioma cell proliferation in vitro and growth of subcutaneously transplanted tumor in vivo. [score:7]
miR-182 and miR-381 silencing induced BRD7 down-regulation by targeting LRRC4. [score:6]
Mutant, nuclear protein+200×mutant probe + wild biotin-probe; Competitor, nuclear protein +200×competitor wild probe + wild biotin-probe; No extracts, no nuclear protein + wild biotin-probe; Mock, nuclear protein+ wild biotin-probe; PD98059, nuclear protein with PD98059 + wild biotin-probe; LY294002, nuclear protein with PD98059 + wild biotin-probe; Scrambled, nuclear protein of transfected miRNA negative control + wild biotin-probe; LNA-182, nuclear protein of transfected LNA-miR-182 inhibitors + wild biotin-probe; LNA-381, nuclear protein of transfected LNA-miR-381 inhibitors + wild biotin-probe; 182M, nuclear protein of transfected miR-182 mimics + wild biotin-probe; 381M, nuclear protein of transfected miR-381 mimics + wild biotin-probe. [score:5]
In addition, to determine whether the miR-182 and miR-381 silencing -induced effects on the expressions of AP2, SP1, E2F6, and c-Myc were LRRC4 -dependent, we performed LRRC4 overexpression studies. [score:5]
ISH and IHC indicated that LNA-anti-miR-381 and/or LNA-anti-miR-182 treatment increased the expression of LRRC4 and reduced the expression of BRD7 (Figures 4B and S4B). [score:5]
To further test the effects of miR-182 and miR-381 on endogenous LRRC4 and BRD7 expressions, we used simple systemic delivery of an unconjugated, PBS-formulated LNA-anti-miR to antagonize expression of endogenous miR-182 and -381 in U251 cells (Figure 5A). [score:5]
miR-182 and miR-381 silencing decreased the expression and activity of AP2, SP1, and E2F6, but increased the expression and activity of c-Myc. [score:5]
We found that the expressions of miR-182, miR-381 or BRD7 proteins were inversely correlated with expression of LRRC4 in glioma tissues and normal brain tissues (Figure 2A). [score:5]
On the basis of our previous research that LRRC4 is a target gene of miR-381, we confirmed LRRC4 is also the target gene of miR-182. [score:5]
The inhibitory effect of the combination treatment with miR-182+miR-381 inhibitors was more robust than single treatments (Figures 4A and S4A). [score:5]
Although BRD7 was predicted as a putative target of miR-381, the miRNA did not combine with the 3′-UTR of BRD7 and the gene sequence was not a bona fide target. [score:5]
0084146.g002 Figure 2miRNA-182 and miR-381 or BRD7 expression is inversely related to LRRC4 expression in gliomas. [score:5]
When the glioma-related LRRC4 gene was queried by TargetScan and PicTar software, it was identified as a target gene of miR-182 and miR-381. [score:5]
miRNA-182 and miR-381 or BRD7 expression is inversely related to LRRC4 expression in gliomas. [score:5]
Mutant, nuclear protein +200×mutant probe + wild biotin-probe; Competitor, nuclear protein +200×competitor cold probe + wild biotin-probe; No extracts, no nuclear protein + wild biotin-probe; Scrambled, nuclear protein of transfected miRNA negative control + wild biotin-probe; LNA-182, nuclear protein of transfected LNA-miR-182 inhibitors + wild biotin-probe; LNA-381, nuclear protein of transfected LNA-miR-381 inhibitors + wild biotin-probe; LRRC4, nuclear protein of transfected LRRC4 gene + wild biotin-probe. [score:5]
The study presented herein demonstrated that LNA -mediated miR-182 and miR-381 silencing in gliomas blocked cell cycle progression in the G0/G1 phase by regulating pRb and E2F3 and inhibited cell proliferation in vitro and growth in vivo. [score:4]
Previous studies have demonstrated that LRRC4, a regulator of miR-182 and miR-381, can inhibit glioma tumorigenicity by modulating receptor tyrosine kinase (RTK) signaling pathways, such as the K-Ras/p-c-Raf/ERK/MAPK and PI-3K/AKT signaling pathways [4], [6]. [score:4]
miR-182 and miR-381 expression levels were assessed by ISH. [score:3]
The ectopic miR-381 mimic promoted the proliferation of glioma cells and LNA -mediated miR-381 silencing inhibited it. [score:3]
Thus, miR-182 and miR-381 may represent useful therapeutic targets for treatment of these tumors. [score:3]
In the present study, we demonstrated that LNA -mediated miR-182 and miR-381 silencing can affect the expression and activity of transcription factors that have binding sites in the BRD7 promoter, including AP2, SP1, E2F6, and c-Myc. [score:3]
In addition, there was a positive correlation found between expressions of miR-182 or miR-381 and BRD7 in all glioma tissues, and normal brain tissues. [score:3]
We further found that the expression of miR-182 and miR-381 or BRD7 and LRRC4 were negatively correlated with the pathological progression of gliomas. [score:3]
Specifically, we analyzed the expression and/or the activation of some of the proteins involved in the K-Ras/p-c-Raf/ERK/MAPK and PI-3K/AKT signaling pathways in response to miR-182 and miR-381 silencing. [score:3]
miR-182 and miR-381 were also determined to be involved in the pathological progression of astrocytoma by targeting LRRC4. [score:3]
LRRC4 has been characterized as a tumor suppressor gene involved in glioma formation [4], and our previous study indicated that LRRC4 is a target of miR-381 [17]. [score:3]
Magnetic resonance imaging (MRI) revealed that administration of miR-182 or miR-381 inhibitors was accompanied by significantly reduced growth of the intracranial transplanted tumors. [score:3]
To evaluate the relevance of the endogenous expressions of miR-182, miR-381, BRD7, and LRRC4, we assessed their expressions in human glioma tissues, as well as in normal brain tissues. [score:3]
In the current study, LNA -mediated miR-182 and miR-381 silencing was applied and found to restore the expression of LRRC4 in gliomas. [score:3]
The results indicated that expression change of miR-182 and miR-381 in normal brain tissue and different grade gliomas (I: 10 cases; II: 22 cases; III: 23 cases; IV: 12 cases) was consistent to that detected by ISH (Figure 2 A-C). [score:3]
miR-182, miR-381, BRD7 are inversely correlated with LRRC4 expression in gliomas. [score:3]
As shown in Figure S2, qRT-PCR was used to furhter verify the expression levels of miR-182 and miR-381 in 19 normal brain tissue samples and 67 primary gliomas. [score:3]
miR-182 and miR-381 silencing inhibited glioma tumorigenicity and induced differentiation. [score:3]
Figure S2 qRT-PCR analysis showing miRNA-182 and miR-381 expression in normal brain and WHO grade I, II, III astrocytomas, and grade IV glioblastoma. [score:3]
To directly test the functional roles of miR-182 and miR-381 in cell proliferation, ectopic miR-182 and miR-381 mimics or LNA-anti-miR-182 and -381 oligonucleotides were transfected into multiple glioma cell lines. [score:2]
miR-182 and miR-381 silencing regulated AP2/SP1/E2F6/c-Myc -mediated BRD7 transcription induced by LRRC4 -mediated K-Ras/c-Raf/ERK/MAPK and PI-3K/AKT signaling pathways. [score:2]
However, compared with treatment with either LNA-anti-miR-182, LNA-anti-miR-381 or 5-Aza-dC alone, the combination treatment of LNA-anti-miR-182/5AZa, LNA-anti-miR-381/5AZa, or LNA-anti-miR-182/LNA-anti-miR-381 did not induce any obvious differences in the growth inhibition of U251 cells (Figure S3). [score:2]
The miR-182 mimic (sense: 5′-UUUGGCAAUGGUAGAACUCACACU-3′; anti-sense: 5′-UGUGAGUUCUACCAUUGCUAAAUU-3′), miR-381 mimic (sense: 5′-UAUACAAGGGCAAGCUCUCUGUTT-3′; anti-sense: 5′-ACAGAGAGCUUGCCCUUGUCGCTT-3′), scrambled mimic (sense: 5′-UUCUCCGAACGUGUCACGUTT-3′; anti-sense: 5′-ACGUGACACGUUCGGAGAATT-3′), anti-miR-182 LNA oligonucleotide (5′-LNA-AGUGUGAGUUCUACCAUUGCCAAA-3′), miR-381 LNA oligonucleotide (5′-LNA-ACAGAGAGCUUGCCCUUGUAUA-3′), and scrambled LNA oligonucleotide (5′-LNA-CAGUACUUUUGUGUAGUACAA-3′) were synthesized by GenePharma and were transfected into cells using Lipofectamine 2000. [score:1]
More importantly, we also found that miR-182, miR-381 and BRD7 were inversely correlated with LRRC4 in astrocytomas of various pathological grades (Figure 2B, C), and the extent of correlation increased from WHO grade I to IV. [score:1]
Treatment with PD98059 or LY294002 abrogated the effects induced by the miR-182 and miR-381 mimics (Figure 6C). [score:1]
miR-182 or miR-381 mimics and LNA -modified Anti-miR-182 or -381 oligonucleotide transfection. [score:1]
LNA-anti-miR-182 or LNA-anti-miR-381. [score:1]
The precise roles of miR-182 and miR-381 in relation to LRRC4 expression in gliomas were investigated by the miRNA silencing tool of locked nucleic acids. [score:1]
pMIR-REPORT vectors harboring wild-type (WT) or mutant 3′-UTR LRRC4 sequences were co -transfected into cells along with the miR-182 or miR-381 constructs using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). [score:1]
miR-182 or miR-381 miRCURY™ LNA custom detection probes (Exiqon, Vedbaek, Denmark) were used for ISH. [score:1]
In contrast, LNA-anti-miR-381 and miR-381 mimics transfection significantly decreased the proliferation of all of these cell lines within 48 h (Figure 3A). [score:1]
Figure S1 miR-381 did not combine with the 3′-UTR of BRD7. [score:1]
These results indicated that miR-182 and miR-381 silencing interfered with or promoted the binding of various transcription factors to the BRD7 promoter. [score:1]
The transplanted rats were treated with intraperitoneal injections of 200 µL of 0.9% saline solution containing: 2 µg of scrambled, LNA-anti-miR-182, or LNA-anti-miR-381, or 1 µg of LNA-anti-miR-182+1 µg of LNA-anti-miR-381 over one day. [score:1]
Aliquots of 200 µL of 0.9% saline solution containing 2 µg of scrambled, LNA-anti-miR-182, or LNA-anti-miR-381, or 1 µg of LNA-anti-miR-182+1 µg of LNA-anti-miR-381 were administered via intraperitoneal injection for one day. [score:1]
It was also found that LNA -mediated miR-182 and miR-381 silencing induced marked differentiation of tumor cells towards a non-cancerous status. [score:1]
Spearman's correlation test was used to evaluate the pairwise expression correlation between miR-182, miR-381, BRD7 and LRRC4 in gliomas. [score:1]
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2
[+] score: 26
To determine whether the aforementioned miRNAs identified in rat lens explant system are also expressed during mammalian lens development in vivo, we conducted ISH analysis of miR-9, miR-143, miR-155, miR-301a, miR-381, and miR-455 in E14.5 and newborn (P0) lenses. [score:4]
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]
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]
At this stage both miR-381 (H) and miR-455 (J) expression domains are restricted to the equatorial zone of the lens in proliferating, migrating, and differentiating lens cells. [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]
The miR-381, miR-495, miR-543, and miR-382 form a miRNA-gene cluster on rat chromosome 6q32. [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]
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]
The miR-495 and miR-543 are neighbors, and miR-381 is located ~12.7 kb from miR-495. [score:1]
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]
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3
[+] score: 17
mir-200a, mir-34, mir-195, and mir-381-3p are usually downregulated in presence of SIRT1 expression, and vice versa low expression of SIRT1 relates to miRNAs upregulation [9, 11, 17, 18, 26– 28]. [score:11]
Also, upregulation of mir-34c-5p and mir-381-3p that target Nampt, an enzyme involved in the production of NAD, the cofactor for SIRT1 [29], diminishes SIRT1 actions. [score:6]
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4
[+] score: 11
Other miRNAs from this paper: 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-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
These miRNAs were chosen as representative of the different patterns that were observed: up-regulation (miR-9a-5p) or down-regulation (miR-598-5p) during latency, down-regulation in the late latency - first spontaneous seizure period (miR-381-3p) and down regulation in the chronic stage (miR-142-5p). [score:11]
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5
[+] score: 10
Figure 8Modulation of miR19a, miR23a, miR130a, miR224, miR381 and miR384-5p expression after siAQP4 and siCx43 treatment. [score:3]
Interestingly, even though not significant, miR130a, miR381 and miR384-5p also exhibited decreased expression in the siCx43 -treated animals of 33%, 11% and 14%, respectively. [score:3]
We chose the most conserved miRNAs between species and selected 6 miRNAs: miR19a, miR23a, miR130a, miR224, miR381, and miR384–5p (see Table 1). [score:1]
No significant difference was observed between control and siAQP4 animals for miR130a or miR381. [score:1]
We chose to study 6 miRNAs, among those most conserved between species: miR19a, miR23a, miR130a, miR224, miR381, and miR384–5p. [score:1]
AQP4 Cx43 Homo sapiens Mus musculus Rattus norvegicus Homo sapiens Mus musculus Rattus norvegicus miR19a ● ● ● ● ○ ○ ○ miR23a ● ● ● ● ○ ○ ○ miR130a shown to repress transcriptional activity of AQP4 M1 promoter* ● ● ● miR224 ● ● ● ● miR381 ● ● ● ● miR384-5p ● ● ● ● ○ ○ ○● based on microrna. [score:1]
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6
[+] score: 10
miR-381-3p suppresses the proliferation of oral squamous cell carcinoma cells by directly targeting FGFR2. [score:6]
miR381-3p is related to suppressive tumor proliferation (Xiao et al., 2017). [score:3]
Finally, as Table 1 showed, seven differentially expressed miRNAs were picked out complying with fold change (fc)≥4 (or ≤1/4) (both Sham group and YQFM group compared to MI group) and Reverse Rate (RR) (YQFM group compared to MI group) between 1 and 2. Finally, miR-21-3p, miR216-5p, miR219a-2-3p, miR381-3p, miR466c-5p, miR542-3p, and miR-702-5p were considered as the differentially reversed miRNAs regulated by YQFM. [score:1]
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7
[+] score: 8
Similarly, when pri-mir-21, pri-mir-199a, and pri-mir-381 primary transcripts were up-regulated, their mature miRNA forms were up-regulated as well (Figure 6). [score:7]
pri-mir381 forward: 5'-tggtacttaaagcgaggttgc-3', pri-mir381 reverse: 5'-ggtcatgcacacacataccac-3'. [score:1]
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8
[+] score: 7
For instance, elevated expression of miR-1297 [30], miR-765 [31] and miR-381 [32] promote NSC proliferation and differentiation through inhibiting HES1 expression. [score:7]
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9
[+] score: 7
Other miRNAs from this paper: rno-mir-186, rno-mir-709
Two miRNAs, miR-186 and miR-381, were up-regulated, while miR-709 was down-regulated. [score:7]
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10
[+] 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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11
[+] score: 1
Except for one (miR-381-5p), none of the miRNAs in this subset showed any main effects of gender (Datasheet S1 in). [score:1]
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12
[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Three miRNA candidates (bta-un10, bta-un13 and bta-un20) were identified in the 5' arm of bta-mir-381, -495 and -487a, respectively, while only the 3' arms of these miRNAs were reported in several species (Table 2, Additional file 4). [score:1]
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[+] score: 1
The miR-381-3p, miR-548u, miR-411-5p, miR-148a-5p, and miR-96-5p which were filtered in HFD comparison but not in intact comparison and no-T2D comparison might involve the progress of T2D fed with HFD only. [score:1]
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