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47 publications mentioning ssc-mir-1

Open access articles that are associated with the species Sus scrofa and mention the gene name mir-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 204
Other miRNAs from this paper: ssc-mir-133a-1, ssc-mir-206, ssc-mir-133b, ssc-mir-133a-2
The SFRP1 3′-UTR sequence around the miRNA-1/206 target sites and the seed sequence of mature miRNA-1/206 are well conserved in mammals, which suggests that the target region is important in SFRP1 regulation and that the regulation of SFRP1 by miRNA-1/206 may also exist in other species. [score:7]
SFRP1 miRNA-206 miRNA-1 Skeletal muscle Development Pig The Wnt signaling pathway plays an essential role during embryonic and postnatal muscle development [1, 2] because it regulates the expression of myogenic regulatory factors, which are essential for myogenic lineage progression and the formation of functional multinucleated myotubes [3, 4]. [score:7]
To further explore the biological functions and regulatory mechanisms of SFRP1 gene and miRNA-1/206 in porcine muscle development, we analyzed the temporal and spatial expression patterns of miRNA-206 and SFRP1 in prenatal and postnatal skeletal muscle at 20 developmental stages. [score:6]
To discover potential targets of miRNA-1/206 during swine myogenesis, we conducted GO and KEGG pathway analyses of targets based on the prediction data. [score:5]
miRNA-1 and miRNA-133 are expressed in both cardiac and skeletal muscles [25] and miRNA-206 is only expressed in skeletal muscle [26]. [score:5]
These results indicated that the target binding site was specific and unique in pigs, and that miRNA-1/206 might repress SFRP1 expression by degrading the mRNA transcripts. [score:5]
In summary, we predicted the target genes of miRNA-1/206 and performed a functional annotation of the target genes. [score:5]
The candidate targets of miRNA-1/206 were predicted using TargetScan and PicTar programs. [score:5]
SFRP1 is a putative target of microRNA-1/206The prediction from the miRNA-mRNA profiles and bioinformatics suggested that SFRP1 was potentially a miRNA-1/206 target in pigs. [score:5]
We predicted the targets of miRNA-1/206 with the TargetScan and PicTar programs. [score:5]
Co -expression analysis of SFRP1 and microRNA-1/206Tang et al. have explored the spatial and dynamic expression of miRNA-1 in the Tongcheng pig (Figure  4D) [35]. [score:5]
According to their study and this study, miRNA-1 and miRNA-206 were abundantly expressed in skeletal muscle and weakly expressed in other tissues. [score:5]
We performed a temporal-spatial expression analysis of SFRP1 mRNA and miRNA-206 in Tongcheng pigs (a Chinese indigenous breed) by quantitative real-time polymerase chain reaction, and conducted the co -expression analyses of SFRP1 and miRNA-1/206. [score:5]
This study demonstrated that SFRP1 expression was regulated by miRNA-1/206. [score:4]
To validate whether SFRP1 was directly targeted by miRNA-1/206 in pigs, we constructed the psiCheck2- SFRP1-3′-UTR, a luciferase reporter vector. [score:4]
miRNA-1 and miRNA-206 were abundant in the postnatal stages and were at low levels in the prenatal stages of muscle development, while SFRP1 exhibited an opposite expression patterns. [score:4]
A significant negative correlation was observed between the expression of miR-1/206 and SFRP1 during porcine skeletal muscle development (p <0.05). [score:4]
Moreover, we explored the interactions between SFRP1 and miRNA-1/206 at the protein level, and confirmed that SFRP1 was significantly down-regulated by miRNA-1/206. [score:4]
Integrated analysis of miRNA and mRNA suggested that SFRP1 and miRNA-1/206 exhibited opposite expression patterns and potentially interacted during prenatal skeletal muscle development. [score:4]
These results indicated that SFRP1 expression might be regulated by miR-1/206 in pigs. [score:4]
miRNA-1/206 promoted skeletal muscle satellite cell proliferation and differentiation [27] and SFRP1 might inhibit myoblast differentiation [12]. [score:3]
Our recent study documented that miRNA-1 and miRNA-206 were abundantly and specifically expressed in porcine skeletal muscle [30]. [score:3]
The temporal expression patterns of miRNA-1/206 and SFRP1 in Tongcheng pigs were consistent with these previous findings. [score:3]
SFRP1, a secreted antagonist of the Wnt-Frizzled pathway, was predicted to be a target of miRNA-1/206 and to participate in the Wnt signaling pathway. [score:3]
To understand the function of SFRP1 and miRNA-1/206 in swine myogenesis, we first predicted the targets of miRNA-1/206 with the TargetScan and PicTar programs, and analyzed the molecular characterization of the porcine SFRP1 gene. [score:3]
These results suggested that the SFRP1 gene was a target of miRNA-1/206. [score:3]
Figure 8 Validating SFRP1 as a positive target for miRNA-1 and miRNA-206. [score:3]
SFRP1 is a putative target of microRNA-1/206. [score:3]
Therefore, the SFRP1 gene, which was predicted to be a target of miRNA-1/206 and was involved in the Wnt signaling pathway, was selected for further study. [score:3]
The bioinformatics analysis predicted SFRP1 to be a target of miRNA-1/206. [score:3]
MicroRNA-1/206(miRNA-1/206) is specifically expressed in skeletal muscle and play a critical role in myogenesis. [score:3]
Co -expression analysis of SFRP1 and microRNA-1/206. [score:3]
miRNA-1 expression in Tongcheng pigs is cited from Tang et al. [35]. [score:3]
Our results indicate that the SFRP1 gene is regulated by miR-1/206 and potentially affects skeletal muscle development. [score:3]
Few reports have considered miRNA-1/206 targets during skeletal muscle development in vivo, particularly in pigs. [score:3]
cgi) programs were used to predict the targets and binding sites of miRNA-1/206. [score:3]
We propose that SFRP1 is regulated by miRNA-1/206, is >involved in the proliferation of muscle cells, and affects prenatal skeletal muscle development. [score:3]
The co -expression analysis revealed that the SFPR1 mRNA was significantly negatively correlated with miRNA-1 (Pearson’s R SFRP1/miRNA-1 = −0.928, p [value] = 0.003) (Figure  5A) and miRNA-206 (Pearson’s R SFRP1/miRNA-1 = −0.922, p [value] = 0.003) (Figure  5B) at the mRNA level in different tissues adult tissues. [score:3]
The miRNA-mRNA profiles and bioinformatics study suggested that the SFRP1 gene was potentially regulated by miRNA-1/206 during porcine skeletal muscle development. [score:3]
Target prediction of miRNA-1/206 and bioinformatic analysis. [score:3]
Tang et al. have explored the spatial and dynamic expression of miRNA-1 in the Tongcheng pig (Figure  4D) [35]. [score:3]
The seed sequence of miRNA-1/206 and the target -binding site between SFRP1 and miRNA-1/ 206 were highly conserved across mammals (Figure  7). [score:3]
Figure 1 Top 10 GO biological process terms significantly enriched in for target genes of miRNA-1/206. [score:3]
Figure 6 SFRP1 3′-UTR has miR-1/206 target binding sites. [score:3]
Figure 5 Correlation analyses of miRNA-1/206 and SFRP1 expression. [score:3]
The prediction from the miRNA-mRNA profiles and bioinformatics suggested that SFRP1 was potentially a miRNA-1/206 target in pigs. [score:3]
Finally, we verified that porcine SFRP1 was a target of miRNA-1/206 using dual luciferase and Western blot assay. [score:2]
Three miRNAs, miRNA-1, −133 and −206, are specifically expressed in muscle and are considered to be myomiRs [23, 24]. [score:2]
miRNA-1 and miRNA-206 regulate skeletal muscle satellite cell proliferation and differentiation by repressing the paired box 7 (Pax7) gene [27]. [score:2]
Figure 9 The miRNA-1 and miRNA-206 regulate SFRP1 at the protein level. [score:2]
These results increase our understanding of the biological functions of SFRP1 and miRNA-1/206 in skeletal muscle development. [score:2]
Dual luciferase assay and Western-blot results demonstrated that SFRP1 was a target of miR-1/206 in porcine iliac endothelial cells. [score:2]
However, in contrast to SFRP1, miRNA-1/206 exhibited a relatively higher level of expression in postnatal muscle compared with prenatal muscle. [score:2]
Correlation analysis revealed that the SFPR1 was significantly negatively correlated with miRNA-1/206 (p < 0.05), and these results indicate that SFRP1 is potentially regulated by miRNA-1/206. [score:2]
We performed a molecular characterization analysis of the porcine SFRP1 gene,, which was one of the predicted targets for miRNA-1/206. [score:1]
The luciferase activity of psiCHECK-2 containing the SFRP1 3′-UTR sequence was significantly decreased by co-transfection with miRNA-1/206 mimics (p < 0.05). [score:1]
Figure 7 Predicted miRNA-1 and miRNA-206 binding sites (highlighted in red) in the 3′-UTR of SFRP1 showing species conservation. [score:1]
Chemically synthesized miRNA-1/206 or the negative control duplexes (Gene Pharma, Shanghai, China) were transfected into the PIECs in combination with a luciferase reporter containing wild-type or mutant SFRP1 3′UTR using Lipofectamine 2000 reagent(Gibco) in 24-well plates. [score:1]
Then, we determined whether SFRP1 was affected by miRNA-1/206 at the protein level. [score:1]
SFRP1 mRNA was significantly negatively correlated with miRNA-1/206 [Pearson’s R SFRP1/miRNA-1 = −0.445, p [value] = 0.032 (Figure  5C); Pearson’s R SFRP1/miRNA-206 = −0.480, p [value] = 0.049(Figure  5D)]. [score:1]
The values are the average (±SE) levels of SFRP1 mRNA and miRNA-1/206 from three independent experiments normalized to GAPDH and U6, respectively. [score:1]
Cotransfection of porcine pre-miRNA-1 (A) and pre-miRNA-206 (B) or control and porcine SFRP1 UTR-derived psiCHECK-2 construct or mutant in PIEC cells. [score:1]
The interaction between SFRP1 and miRNA-1/206 in pigs has not been previously reported. [score:1]
The porcine SFRP1-CDS-3′-UTR-psiCHECK-2 vector was constructed, and it was co -transfected with miRNA-1 and miRNA-206 mimics in PIECs. [score:1]
The luciferase activity of the psiCHECK-2- SFRP1–3′-UTR (mut) was not significantly decreased by both the miRNA-1 and miRNA-206 mimics (12.39% of control for the miRNA-1 mimic -transfected group and 16.76% of control for the miRNA-206 mimic -transfected group) (p >0.05) (Figure  8). [score:1]
gov/) was performed to investigate the potential biological function and KEGG pathways of miRNA-1/206 targets [31]. [score:1]
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2
[+] score: 58
Other miRNAs from this paper: ssc-mir-133a-1, ssc-mir-133b, ssc-mir-133a-2
Real-time PCR analysis showed that miR-1 expression was significantly up-regulated, whereas miR-133a expression was significantly down-regulated in saline group compared with the sham group, and these effects were attenuated by sildenafil (p < 0.05, Figure  5). [score:10]
Indeed, miRNA-1 is one of the most strongly up-regulated miRNAs, whereas miRNA-133a is one of the down-regulated miRNAs in rat hearts upon acute myocardial I/R. [score:7]
The results of the present study suggested that sildenafil treatment inhibited the increases in the miRNA-1 levels which causes down-regulation of antiapoptotic gene-Bcl-2, whereas alleviated the decreases in the miRNA-133a levels which negatively regulates pro-apoptotic genes. [score:7]
Increased miRNA-1 causes down-regulation of multiple antiapoptotic genes, such as Hsp70, IGF-1 and Bcl-2; whereas miR-133a negatively regulates a pro-apoptotic gene (i. e. caspase-9) [10]. [score:5]
Additionally, sildenafil treatment inhibited the increases in the microRNA-1 levels and alleviated the decreases in the microRNA-133a levels which negatively regulates pro-apoptotic genes. [score:4]
miRNA-1 expression is restricted to heart and skeletal muscle and is regulated by transcription factor [31]. [score:4]
The opposite consequences of miRNA-1/miRNA-133a may be largely attributed to different targets. [score:3]
Figure 5Real-time PCR analysis of relative microRNA-1(a) and microRNA-133a (b) expression. [score:3]
Changes in miRNA-1 and miRNA-133 expression. [score:3]
The major findings of this study are as follows: (1) sildenafil improved post-resuscitation perfusion of the heart, and thus reduced cardiac myocyte apoptosis and improved cardiac function; (2) sildenafil treatment inhibited the increases in the microRNA-1 levels, but alleviated the decreases in the microRNA-133a levels. [score:3]
In particular, miRNA-1 and miRNA-133a have been shown to be regulated after myocardium I/R injury [9]. [score:2]
Recent functional studies indicate that miRNA-1 and miRNA-133a have opposite effects in the regulation of stress -induced myocyte survival, with a pro-apoptotic role of miR-1 and anti-apoptotic role of miRNA-133a. [score:2]
Among the known miRNAs, miR-1 and miR-133 are clustered on the same chromosomal locus and transcribed together as a single transcript, which becomes two independent, mature miRNAs with distinct biological functions. [score:1]
The relative expression of miR-133a and miR-1 were calculated and normalized to U6 using the comparative Ct method. [score:1]
miR-1 and miR-133a level were quantified by the mirVana qRT-PCR (quantitative real-time PCR) miRNA Detection Kit (Ambion, USA) in conjunction with real-time PCR with SYBR Green I (Applied Biosystems, USA), as previously described in detail [20]. [score:1]
Collectively, these data suggest that approaches to either decrease cardiac miR-1 levels or increase miRNA-133 levels during an ischaemic event might potentially attenuate I/R -induced myocardial injury. [score:1]
More recently, miRNA-1 and miRNA-133a were shown to produce opposing effects on oxidative stress-with miRNA-1 being pro-apoptotic and miRNA-133 being anti-apoptotic [10]. [score:1]
[1 to 20 of 17 sentences]
3
[+] score: 51
In selected developmental muscle, while miR-1 and miR-765 were differentially expressed in Tongcheng pigs and 32 miRNAs were differently expressed uniquely in Wuzhishan pigs, only miR-619 was differentially expressed exclusively in Landrace pigs. [score:8]
A previous study suggested that miR-1, miR-133b and miR-206 are associated with skeletal muscle development; we also found that these miRNAs were differentially expressed and critical to prenatal skeletal muscle development. [score:5]
For example, only miR-619 was differentially expressed in Landrace pigs, while miR-1 and miR-765 were differentially expressed in Tongcheng pigs. [score:5]
Using the Targetscan prediction program, for example, a total of 478, 435 and 478 mRNA targets were obtained for miR-1, miR-133 and miR-206, respectively. [score:5]
The SFRP2 gene, which plays an active role in embryogenesis, especially in muscle development 62, was found to be a potential target of miR-1 and miR-206 in myogenesis in Tongcheng pigs. [score:4]
The expression of C9orf19 was potentially regulated by miR-1, miR-133b, miR-206 and let-7a. [score:4]
There were 22, 21, 10, 9 and 9 target mRNAs for miR-765, miR-302b, miR-1, let-7a and miR-206, respectively, suggesting that these miRNAs significantly contribute to prenatal skeletal muscle development in Tongcheng pigs. [score:4]
The target mRNAs of miR-1, 133b and 206 were identified in this study. [score:3]
Eight miRNAs (miR-765, miR-302b, miR-1, let-7a, miR-206, miR-500, miR-546 and miR-705) targeted 86.1% of the mRNAs in Tongcheng pigs. [score:3]
In this study, we identified only 10, 27 and 34 mRNA potential targets for miR-1, miR-133b and miR-206, respectively. [score:3]
FKBP1B and HMGCS1, which encode rate-limiting enzymes of the cholesterol synthesis pathway 61, were potentially regulated by let-7a, miR-1 and miR-206. [score:2]
As shown in Fig. 5, miR-1 potentially regulated 10 mRNAs, including C9orf19, DLG7, FKBP1B, GJA7, HMGCS1, MAP1A, NCALD, PCDH19, RAP2A and SFRP2. [score:2]
The miRNA-GO network analysis suggested that cell adhesion was regulated by six miRNAs (miR-1, miR-206, miR-302b, miR-625, miR-765 and miR-669c). [score:2]
miR-1 was associated with the sterol biosynthetic process, somitogenesis, muscle contraction, the cholesterol biosynthetic process and cell adhesion (Fig. 10). [score:1]
[1 to 20 of 14 sentences]
4
[+] score: 48
The results of transient transfection assays demonstrated that (1) miR-21 negatively regulates the expression of Pitx2c (this work), (2) miR-1 suppresses Myocd expression [53], and (3) miR-10a and miR-10b both inhibit Tbx5 expression [54]. [score:11]
An aspect of particular interest of our study was the finding that the upregulation of miR-1, miR-10a, miR-10b, and miR-21 is negatively correlated with downregulation of, respectively, MYOCD, TBX5, and PITX2c in the paced LA (see Figure 5(e)). [score:7]
Downregulation of miR-1, miR-10a, miR-29a, and miR-208a has been implicated in chronic AF [7, 13, 59], while these miRNAs were highly upregulated in the porcine LA in response to brief paroxysms of AF. [score:7]
In transfection assays, miR-1 inhibits mouse Myocd expression at the transcript [52] and protein level [53], while both miR-10a and miR-10b negatively modulate human Tbx5 expression at the protein level [54]. [score:6]
Computational analysis (by miRanda and Targetscan) of the 3′ untranslated region of pig Pitx2, Tbx5, and Myocd genes revealed consensus sites for binding of, respectively, miR-21, miR-10a/miR-10b, and miR-1 (Figure 5(a)). [score:5]
Consistent with the results obtained and other reports [53, 54], the histogram plot (Figure 5(e)) exhibits a clear inverse correlation in the protein expression of Pitx2 versus miR-21, Tbx5 versus miR-10b, and Myocd versus miR-1 in the LA of paced animals, confirming thus our hypothesis. [score:3]
Pacing -induced alterations in the expression of other miRNAs with particular concern for their involvement in AF could not be determined by microarray hybridizations due to a high variability among replicates (miR-1, miR-21, miR-23a/b, miR-29a, and miR-133a) or very low hybridization signals (miR-10a, miR-10b; see the complete microarray data at NCBI through GEO accession number GSE65330). [score:3]
Our qPCR analysis showed that pacing resulted in a significant upregulation of a set of AF -associated miRNAs (i. e., miR-1, miR-10a, miR-10b, miR-21, miR-29a, and miR-208a) in the LA compared with the control (see Figure 3). [score:3]
Six miRNAs (miR-1, miR-10a-5p, miR-10b, miR-21, miR-29a, and miR-208a) showed a higher expression in paced as compared with nonpaced animals. [score:2]
From this perspective, our data would suggest that higher levels of miR-21, miR-10b, and miR-1 in the LA myocardium contribute to arrhythmogenesis via perturbation of Pitx2, Tbx5, and Myocd signaling pathways, respectively. [score:1]
[1 to 20 of 10 sentences]
5
[+] score: 46
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-22, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-98, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-101a, mmu-mir-126a, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-142a, mmu-mir-181a-2, mmu-mir-194-1, hsa-mir-208a, hsa-mir-30c-2, mmu-mir-122, mmu-mir-143, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-122, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-208a, 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-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29c, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-20a, rno-mir-101b, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-17, mmu-mir-19a, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-19b-1, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-26a-2, hsa-mir-378a, mmu-mir-378a, hsa-mir-326, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19a, rno-mir-22, rno-mir-26a, rno-mir-26b, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30c-2, rno-mir-98, rno-mir-101a, rno-mir-122, rno-mir-126a, rno-mir-130a, rno-mir-133a, rno-mir-142, rno-mir-143, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-194-1, rno-mir-194-2, rno-mir-208a, rno-mir-181a-1, hsa-mir-423, hsa-mir-18b, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, ssc-mir-122, ssc-mir-15b, ssc-mir-181b-2, ssc-mir-19a, ssc-mir-20a, ssc-mir-26a, ssc-mir-326, ssc-mir-181c, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-18a, ssc-mir-29c, ssc-mir-30c-2, hsa-mir-484, hsa-mir-181d, hsa-mir-499a, rno-mir-1, rno-mir-133b, mmu-mir-484, mmu-mir-20b, rno-mir-20b, rno-mir-378a, rno-mir-499, hsa-mir-378d-2, mmu-mir-423, mmu-mir-499, mmu-mir-181d, mmu-mir-18b, mmu-mir-208b, hsa-mir-208b, rno-mir-17-2, rno-mir-181d, rno-mir-423, rno-mir-484, mmu-mir-1b, ssc-mir-15a, ssc-mir-16-2, ssc-mir-16-1, ssc-mir-17, ssc-mir-130a, ssc-mir-101-1, ssc-mir-101-2, ssc-mir-133a-1, ssc-mir-181a-1, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-499, ssc-mir-143, ssc-mir-423, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-98, ssc-mir-208b, ssc-mir-142, ssc-mir-19b-1, hsa-mir-378b, ssc-mir-22, rno-mir-126b, rno-mir-208b, rno-mir-133c, hsa-mir-378c, ssc-mir-194b, ssc-mir-133a-2, ssc-mir-484, ssc-mir-30c-1, ssc-mir-126, ssc-mir-378-2, ssc-mir-451, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, mmu-mir-378b, mmu-mir-101c, hsa-mir-451b, hsa-mir-499b, ssc-let-7a-2, ssc-mir-18b, hsa-mir-378j, rno-mir-378b, mmu-mir-133c, mmu-let-7j, mmu-mir-378c, mmu-mir-378d, mmu-mir-451b, ssc-let-7d, ssc-let-7f-2, ssc-mir-20b-1, ssc-mir-20b-2, ssc-mir-194a, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, rno-let-7g, rno-mir-15a, ssc-mir-378b, rno-mir-29c-2, rno-mir-1b, ssc-mir-26b
Thus, miRNA families (e. g., miR-1 and miR-122) that are specifically or highly expressed in any one of the 3 tissues, or miRNAs that are expressed ubiquitously (e. g., let-7 and miR-26) in all 3 tissues, show a far greater frequency than other miRNAs. [score:5]
These two miRNA genes – miR-1 and miR-133 – exist as a cluster and thus are always expressed together in mouse [42]. [score:3]
In agreement with this observation, miR-1 is the most abundantly expressed miRNA in the heart but not in the liver or thymus (Figure 3), two other tissues used for miRNA library generation. [score:3]
Several miRNAs (miR-1, miR-133, miR-499, miR-208, miR-122, miR-194, miR-18, miR-142-3p, miR-101 and miR-143) have distinct tissue-specific expression patterns. [score:3]
The expression patterns of miR-1 and miR-133 largely overlapped in many tissues examined in this study (Figure 2). [score:3]
Thus, the high abundance of miR-1 as indicated by the number of sequence reads is associated with its high expression in the heart. [score:3]
Our small RNA blot analysis indicated that miR-1 was highly expressed in the heart but moderately in the stomach, testes, bladder and spleen (Figure 2). [score:3]
For instance, the miR-1 family has the highest frequency (411 times) in our sequences (Table 2) and the highest level of expression in the heart, but was barely detected in thymus and liver (Figure 2). [score:3]
Like miR-1, miR-133 is a muscle-specific miRNA (Figure 2) because of its abundant expression in many other muscular tissues such as heart and skeletal muscle [45, 46]. [score:3]
miR-1 is one of the highly conserved miRNAs and found to be abundantly and specifically expressed in the heart and other muscular tissues [41, 42]. [score:3]
Additionally, miR-1 and miR-133 in the heart, miR-181a and miR-142-3p in the thymus, miR-194 in the liver, and miR-143 in the stomach showed the highest levels of expression. [score:3]
For instance, miR-133 is represented only by 4 clones (two reads each for 133a and 133b) in our sequences, which indicates a 100-fold lower expression level compared with that of miR-1 family, if cloning frequency taken as a measure of expression. [score:2]
The miR-1 family is represented by three members (miR-1a, miR-1b and miR-1c) in diverse animals (miRBase). [score:1]
miR-1 was barely detected in the liver, with only trace amounts in the thymus (Figure 2). [score:1]
Therefore the total miR-1 count in our sequences could be derived largely from heart tissue. [score:1]
Our sequence analysis in this study indicated that miR-1 family (miR-1a, miR-1b and miR-1c) has the highest abundance (411 sequence reads). [score:1]
The discrepancies between the cloning frequency and small RNA blot results for miRNA-1 and miR-133 could not be attributed to the RNA source because the same RNA samples were used for both experiments (cloning and small RNA blot analysis). [score:1]
The high level of miR-1 in the pig heart is in agreement with previous reports [43, 44]. [score:1]
However, our small RNA blot analysis indicated a different picture as miR-133 was detected as abundantly as miR-1 in the heart (Figure 2). [score:1]
We cannot ascertain whether the miR-1 family is also represented by three members in pig because of the lack of complete genome information, but is possible because we found miR-1a, miR-1b and miR-1c homologs in our library (Table 2). [score:1]
We also used approximately a similar amount (activity) of [32]P -labelled probe for detection of miR-1 and miR-133. [score:1]
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6
[+] score: 35
For example, miR-1 directly targets HDAC4, a transcriptional repressor of muscle gene expression to promote myogenesis, and miR-133 enhance myoblast proliferation by repressing serum factor (SRF) [40]. [score:6]
miR-133 expression level of MS pigs was always higher than LW (P < 0.05), while miR-1 and miR-206 has not shown obvious expression patterns between these two breeds (Fig 8). [score:5]
The expression levels of miR-133, miR-1 and miR-206 in Large White (LW) and Meishan (MS) pigs during skeletal muscle development at 35 to 90 dpc (E35, E55 and E90). [score:4]
However the expression patterns of miR-1 and miR-206 from 35 to 90 dpc are similar between LW and MS, and significantly affected by developmental stages (P [t] < 0.01). [score:4]
Interestingly, Among them, miR-133, miR-1, miR-206 and miR-148a were highly abundant in MS pigs, while let-7 family, miR-214 and miR-181 were highly expressed in LW. [score:3]
The expression levels of muscle specific miRNAs, including miR-133, miR-1 and miR-206, in longissimus dorsi of LW and MS on pregnancy days 35, 55 and 90 were analyzed. [score:3]
By contrast, miR-1 promotes muscle differentiation by targeting histone deacetylase 4 (HDAC4) [11]. [score:3]
Some myogenesis related miRNAs (miR-133, miR-1, miR-206 and miR-148a) are highly abundant in MS pigs, while other miRNAs (let-7 family, miR-214, miR-181) highly expressed in LW. [score:3]
Finally, the expression patterns of muscle specific miRNA (i. e., miR-1, miR-133 and miR-206) were detected in LW and MS. [score:3]
The difference of miRNAs (miR-133, miR-1 and miR-206) among six samples (the muscle of LW and MS fetus at each time point 35d, 55d and 90d) was analyzed through two-way ANOVA method, in which breeds and time points were factors. [score:1]
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[+] score: 35
A mutation in the myostatin gene of heavily muscled Belgian Texel sheep creates a target site for miR-1 and miR-206 containing RISC complexes in the 3' untranslated portion of the transcript, resulting in decreased translation of the myostatin protein and consequent increase in muscle mass. [score:8]
Expression of the muscle regulatory factor, myogenic factor 5, has been reported to regulate miR-1 and miR-206 transcription level in a chicken cell culture mo del [18]. [score:5]
Based on abundance level, these data suggest that miR-206 and miR-1 may have a greater role in fetal muscle development than miR-133, or their targets are higher in abundance. [score:4]
Data for the satellite cells and adult muscle is presented as the average of multiple transcriptome libraries presented in Additional file 1. In comparison to the high abundance of miR-206 in muscle tissue, porcine miR-1 had relatively moderate abundance that increased throughout development, similar to the pattern observed for this miR in mouse muscle development [16]. [score:3]
Data for the satellite cells and adult muscle is presented as the average of multiple transcriptome libraries presented in Additional file 1. In comparison to the high abundance of miR-206 in muscle tissue, porcine miR-1 had relatively moderate abundance that increased throughout development, similar to the pattern observed for this miR in mouse muscle development [16]. [score:3]
These data suggest that miR-1 and miR-206 play different roles in muscle development, with miR-1 affecting regulation of genes that require inactivation in later fetal stages and miR-206 having a more constant role in repressing genes immediately after differentiation. [score:3]
In contrast to miR-1 and miR-206, miR-133 was detected only at low levels in fetal development yet increased in the neonate and adult (Figure 3). [score:2]
Overall, miR were lowly abundant throughout fetal development with the exception of let-7 and muscle specific miR-1 and miR-206. [score:2]
In addition, miR-1 was moderately abundant throughout developmental stages with highest abundance in the adult. [score:2]
While miR-1 and miR-133 abundance increases during differentiation in cell culture [16], the role of these miR in adult skeletal muscle has yet to be fully determined. [score:1]
MiR-133 increases proliferation of C [2]C [12 ]myoblasts, whereas miR-206 and miR-1 promote differentiation [16]. [score:1]
Three muscle-specific miRNA (miR-1, miR-133, and miR-206) were identified to increase in abundance during muscle cell differentiation [10, 16, 17]. [score:1]
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[+] score: 34
Other miRNAs from this paper: ssc-mir-122, ssc-mir-125b-2, ssc-mir-181b-2, ssc-mir-20a, ssc-mir-23a, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-107, ssc-mir-21, ssc-mir-29c, ssc-mir-30c-2, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-103-1, bta-mir-20a, bta-mir-21, bta-mir-26b, bta-mir-30d, bta-mir-499, bta-mir-99a, bta-mir-125b-1, bta-mir-126, bta-mir-181a-2, bta-mir-199a-1, bta-mir-30b, bta-mir-107, bta-mir-10a, bta-mir-127, bta-mir-142, bta-mir-181b-2, bta-mir-30e, bta-mir-92a-2, bta-let-7d, bta-mir-132, bta-mir-138-2, bta-mir-17, bta-mir-181c, bta-mir-192, bta-mir-199b, bta-mir-200a, bta-mir-200c, bta-mir-214, bta-mir-23a, bta-mir-29b-2, bta-mir-29c, bta-mir-455, bta-let-7g, bta-mir-10b, bta-mir-30a, bta-mir-200b, bta-let-7a-1, bta-let-7f-1, bta-mir-122, bta-mir-30c, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-99b, ssc-mir-99b, ssc-mir-17, ssc-mir-30b, ssc-mir-199b, bta-mir-1-2, bta-mir-1-1, bta-mir-129-1, bta-mir-129-2, bta-mir-133a-2, bta-mir-133a-1, bta-mir-133b, bta-mir-135b, bta-mir-138-1, bta-mir-143, bta-mir-144, bta-mir-146b, bta-mir-146a, bta-mir-181d, bta-mir-190a, bta-mir-199a-2, bta-mir-202, bta-mir-206, bta-mir-211, bta-mir-212, bta-mir-223, bta-mir-26a-1, bta-mir-29d, bta-mir-30f, bta-mir-338, bta-mir-33a, bta-mir-33b, bta-mir-375, bta-mir-429, bta-mir-451, bta-mir-92a-1, bta-mir-92b, bta-mir-29e, bta-mir-29b-1, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-133a-1, ssc-mir-146b, ssc-mir-181a-1, ssc-mir-30a, bta-mir-199c, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-133b, ssc-mir-29a, ssc-mir-30d, ssc-mir-30e, ssc-mir-199a-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-10b, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-99a, ssc-mir-92a-2, ssc-mir-92a-1, ssc-mir-92b, ssc-mir-192, ssc-mir-142, ssc-mir-127, ssc-mir-202, ssc-mir-129a, ssc-mir-455, ssc-mir-125b-1, ssc-mir-338, ssc-mir-133a-2, ssc-mir-146a, bta-mir-26c, ssc-mir-30c-1, ssc-mir-126, ssc-mir-199a-1, ssc-mir-451, ssc-let-7a-2, ssc-mir-129b, ssc-mir-429, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, ssc-mir-132, ssc-mir-138, ssc-mir-144, ssc-mir-190a, ssc-mir-212, bta-mir-133c, ssc-mir-26b, ssc-mir-200b, ssc-mir-223, ssc-mir-375, ssc-mir-33b
Paula et al. (2017) showed that a short period of food restriction significantly increased the expression of miR-1, miR-206, miR-199, and miR-23a in fast muscle and significantly decreased the expression of miR-1 and miR-206 in slow muscle, while their targets (IGF-1 for miR-1, miR-206, and miR-199; mTOR for miR-199; and MFbx and PGC1a for miR-23a) exhibited negatively correlated expression profiles. [score:9]
Some muscle miRNAs have well-defined target genes, as miR-206 regulates IGF-1; miR-1, miR-122, and miR-462 control IGF-2a; the let-7 family regulates MSTN; miR-103 and miR-107 modulate GHR and FSHR; and miR-138 and miR-211 control LHR. [score:5]
In the skeletal muscle, the main edible part of the fish, miR-1, miR-133a, and miR-206 have conserved expression patterns in all farmed fish species, which makes them interesting molecules for modulating muscle development and growth. [score:4]
In tilapia, Yan et al. (2012a) and Nachtigall et al. (2015) showed that miR-1, miR-133a, and miR-206 have similar expression patterns in adult males and females and may assist each other to accurately control the development of skeletal muscles, although they perform distinct biological functions. [score:4]
MiR-1 is responsible for repressing the expression of histone deacetylase 4 (HDAC4), which is a negative regulator of cellular differentiation and thus promotes myocyte differentiation. [score:3]
The expression pattern of 12 miRNAs, including mir-1, mir-133 and mir-206, was validated by real time PCR. [score:3]
Duran et al. (2015) analyzed the impact of the miRNA-target interactions of miR-1/ hdac4, miR-133-a/b/ srf, miR-206/ pax7, and miR-499/ sox6 in fast- and slow-twitch skeletal muscles during growth. [score:3]
MiR-1, miR-133a, miR-133b, miR-206, and miR-499 have been shown to be involved in the control of genes related to myoblast proliferation and differentiation. [score:1]
The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiation. [score:1]
They found that miR-1 and miR-206 may promote myoblast differentiation in fast- and slow-twitch muscles in adult individuals, while miR-133a/b acts earlier, promoting myoblast proliferation in juveniles. [score:1]
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[+] score: 30
miR-1, a muscle-specific microRNA, promotes cell apoptosis by targeting Bcl-2 (Tang et al., 2009), and could target heat shock protein 70 (HSP70) in the development of muscle atrophy (Kukreti et al., 2013). [score:6]
Besides the miR-1 and miR133a that we found highly expressed in all the stages (McCarthy & Esser, 2007), miR-26a also showed abundant expression (Huang, Sherman & Lempicki, 2008; Huang et al., 2008). [score:5]
miR-27b showed increasing expression levels during development, and miR-1 showed the opposite trend. [score:4]
Hence, miR-1 could be a potential modulator in regulating porcine postnatal skeletal muscle development. [score:3]
Previous study performed by Qin et al. indicated that most of the highly expressed miRNAs in porcine skeletal muscle such as miR-1 and miR-133 will be more functional. [score:3]
Therefore, miR-27b promotes myogenesis and proliferation, whereas miR-1 inhibits these processes and induces apoptosis. [score:3]
Particularly, miR-1 showed significantly increasing expression level in 180d and 7y stages (Fig. 5A and Table S7). [score:3]
Of these miRNAs, six (miR-133a-1/-2-3p, let-7a-1/-2-5p, miR-27b-3p, miR-26a-5p, miR-1-3p, and let-7f-1/-2-5p) were shared by all five stages and were closely related to myogenesis, cell growth, myocyte proliferation, and cell apoptosis. [score:1]
By using both C2C12 myotubes and dex -induced muscular atrophy mouse mo dels, Kukreti et al. (2013) indicated that miR-1 is a muscle-specific microRNA and has a role in promoting muscle atrophy. [score:1]
On the other hand, McCarthy & Esser (2007) also revealed that miR-1 decreased during mouse skeletal muscle hypertrophy. [score:1]
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[+] score: 30
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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-208a, hsa-mir-148a, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-214, hsa-mir-221, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-23b, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-206, hsa-mir-1-1, hsa-mir-128-2, hsa-mir-29c, hsa-mir-26a-2, hsa-mir-378a, hsa-mir-148b, hsa-mir-133b, hsa-mir-424, ssc-mir-125b-2, ssc-mir-148a, ssc-mir-23a, ssc-mir-24-1, ssc-mir-26a, ssc-mir-29b-1, ssc-mir-181c, ssc-mir-214, ssc-mir-27a, ssc-let-7c, ssc-let-7f-1, ssc-let-7i, ssc-mir-103-1, ssc-mir-128-1, ssc-mir-29c, hsa-mir-486-1, hsa-mir-499a, hsa-mir-503, hsa-mir-411, hsa-mir-378d-2, hsa-mir-208b, hsa-mir-103b-1, hsa-mir-103b-2, ssc-mir-17, ssc-mir-221, ssc-mir-133a-1, ssc-mir-503, ssc-mir-181a-1, ssc-mir-206, ssc-let-7a-1, ssc-let-7e, ssc-let-7g, ssc-mir-378-1, ssc-mir-133b, ssc-mir-29a, ssc-mir-199a-2, ssc-mir-128-2, ssc-mir-499, ssc-mir-143, ssc-mir-10a, ssc-mir-486-1, ssc-mir-103-2, ssc-mir-181a-2, ssc-mir-27b, ssc-mir-24-2, ssc-mir-23b, ssc-mir-148b, ssc-mir-208b, ssc-mir-424, ssc-mir-127, ssc-mir-125b-1, hsa-mir-378b, hsa-mir-378c, ssc-mir-411, ssc-mir-133a-2, ssc-mir-126, ssc-mir-199a-1, ssc-mir-378-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-499b, ssc-let-7a-2, ssc-mir-486-2, hsa-mir-378j, ssc-let-7d, ssc-let-7f-2, ssc-mir-29b-2, hsa-mir-486-2, ssc-mir-378b
Notably, in addition to porcine myomiRs (miR-1, -206, -133 a-3p/a-5p/b), three other miRNAs (miR-128, -208b and -378) reported to be related to muscle development in other mammals were also included in up-regulation Cluster 2, suggesting their roles in the regulation of porcine embryonic myogenesis at 35 to 77 dpc. [score:6]
Journal of Cell Science 120: 3045-3052 74 Yan D, Dong XD, Chen XY, Wang LH, Lu CJ et al. (2009) MicroRNA-1/206 Targets c-Met and Inhibits Rhabdomyosarcoma Development. [score:5]
STEM clustering results suggested that ssc-miR-378 functioned as a new candidate miRNA for porcine myogenesis because of its expression profile similar to ssc-miR-1 and -133a-3p (Figure 5A). [score:3]
It’s worth noting that many miRNAs are expressed in a tissue-specific or stage-specific manner [10], and the best-characterized muscle-specific miRNAs (myomiRs [11]) are miR-1, miR-206 and miR-133 families which specifically expressed in cardiac and skeletal muscles. [score:3]
Stem-loop quantitative RT-PCR was then performed on 9 random miRNAs with different expression levels (miR-1, -206, -133a-3p, -133a-5p, -133b, -378, -214, -744 and let-7f) to validate the sequencing data (Figure 6). [score:3]
The predominance of miR-1 is consistent with its well established function during skeletal muscle development [21] and reported role during porcine myogenesis [22]. [score:2]
Ssc-miR-1 was the most abundant miRNA in ten libraries, consistent with the well-established function of miR-1 during skeletal muscle development [21]. [score:2]
In addition, we both focused on the changes in abundance of myomiRs (miR-1, -206 and -133) during swine skeletal muscle development. [score:2]
Figure 2 showed that the number of DE miRNAs during myofiber formation was the least but still accounted for almost 50% of total DE miRNAs, from which all of porcine myomiRs (ssc-miR-1, -206, -133 a-3p/a-5p/b) were identified. [score:1]
Intriguingly, 11 of the 25 common miRNAs were reported to function as muscle-related miRNAs including the well-known myomiRs (miR-1, -206 and -133 family). [score:1]
In addition to the best-studied myomiRs (miR-1, -206 and miR-133 families), 11 other DE muscle-related miRNAs (miR-378 [24], miR-148a [27], miR-26a [28, 29], miR-27a/b [30, 31], miR-23a [32, 33], miR-125b [34], miR-24 [35], miR-128 [36], miR-199a [37] and miR-424 [38]) with high abundance (average RPM >1,000) and another 14 (miR-181a/b/c/d-5p [26], miR-499-5p [11], miR-503 [38], miR-486 [39], miR-214 [40], miR-29a/b/c [41– 43], miR-221/222 [44] and miR-208 [11] with low abundance (average RPM <1,000) were detected in myogenesis of pig. [score:1]
The most abundant miRNA was ssc-miR-1, which presented by more than 2,100,000 RPM in ten libraries. [score:1]
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[+] score: 28
In C2C12 myoblast, miR-1 suppresses the expression of HDAC and promotes myoblast differentiation [5]. [score:5]
We found that miR-1 was expressed at higher levels on D100 and that miR-378 was expressed at higher levels on E90. [score:5]
The miR-1 regulates skeletal muscle development by targeting CNN3 in pigs [19]. [score:5]
These data were consistent with the previously described role of miR-1 in regulating skeletal muscle satellite cell proliferation and differentiation by repressing Pax7 and that of miR-378 in targeting the myogenic repressor MyoR during myoblast differentiation [26, 40]. [score:4]
The distribution of the top most abundant 15 miRNAs in our Solexa sequencing analysis are shown in Table 1. Of these, ssc-miR-206 had the highest reads in the E90 libraries, and ssc-miR-1 was highly expressed at D100. [score:3]
In particular, the miR-1/206 and miR-133a/133b families contribute to the development of myocardial and skeletal muscles [3, 4]. [score:2]
Four miRNAs (ssc-miR-29a, ssc-miR-1, ssc-miR-128, ssc-miR-320) showed obviously enhanced expression at D100 compared to E90. [score:2]
These two miRNAs were considered to be myomiRs, and the data herein confirmed that ssc-miR-206 and ssc-miR-1 play vital roles in muscle development. [score:1]
Aside from ssc-miR-206 and ssc-miR-1, ssc-miR-378 was the most abundant at E90, followed by ssc-miR-143-3p, ssc-let-7a, ssc-let-7f, ssc-let-7c, ssc-miR-30d, ssc-miR-30a-5p, ssc-miR-10b, ssc-miR-127, ssc-miR-148a, ssc-miR-126, ssc-miR-7i, and ssc-miR-21. [score:1]
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[+] score: 25
MiR-1 and miR-133 are expressed both in cardiac and skeletal muscles [22], whereas miR-206 is expressed only in skeletal muscles [23], [24]. [score:5]
Ssc-miR-206 was expressed only in skeletal muscles, while ssc-miR-1 was expressed only in the skeletal muscles and heart. [score:5]
Although an increasing body of evidence shows that miRNAs play important roles in the regulation of skeletal muscle development, precise regulatory mechanisms of the biological functions of most miRNAs remain unclear, and most research is restricted to myomiRs, such as miR-1, miR-133 and miR-206. [score:4]
Nielsen et al. [21] showed that ssc-miR-1 and ssc-miR-206 are expressed at extremely high levels in the longissimus muscles of Danish Landrace/Yorkshire crossbred pigs of age 1.5–2 years; however, the abundance of other miRNAs was relatively low. [score:3]
MiR-1, miR-206 and miR-133 are classified as myomiRs, as they play important roles in the regulation of muscle development and differentiation. [score:3]
The qPCR results of ssc-miR-1 and ssc-miR-206 were consistent with previous reports. [score:1]
Although ssc-miR-133, another type of myomiR, could also be detected in our Solexa results, the reads were moderate and were not as abundant as that of ssc-miR-1 and ssc-miR-206. [score:1]
Ssc-miR-206, ssc-miR-1 and ssc-miR-378 had the most reads in our Solexa results. [score:1]
Previous experiments showed that miR-1 and miR-206 promoted the differentiation of myoblasts, while miR-133 promoted proliferation [1], [2]. [score:1]
In our results, the abundance of ssc-miR-1 and ssc-miR-206 was extremely high, which was consistent with their results. [score:1]
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[+] score: 22
Other miRNAs from this paper: ssc-mir-26a, ssc-mir-27a, ssc-mir-29a, ssc-mir-27b, ssc-mir-26b
Expressions of ANP, BNP, and miRNA-29a were up-regulated, while SERCA2a and miRNA-1 were down-regulated. [score:9]
b Significant alteration of the miRNA expression pattern was detected, including down regulation of miR-1 and upregulation of miR-29a in both ventricles. [score:7]
Fig.  8Molecular proof of cardiac hypertrophy and fibrosis, by myocardial gene expression of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and SERCA2a and microRNA-1 and 29 expression in left (LV) and right ventricle (RV) of pigs with cardiac hypertrophy compared to controls. [score:4]
The microRNA-1 is well documented to be decreased in heart failure and fibrosis as well as animal mo dels of cardiac hypertrophy, similar to our mo del [24, 25]. [score:1]
We found depletion of the cardiomyocyte growth-repressing miR-1 to 50–66% in both the LV and RV of pigs with cardiac hypertrophy (Fig.   8b). [score:1]
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[+] score: 17
Recent studies showed that miR-1 promotes myogenesis by targeting histone deacetylase 4 (HDAC4), a transcriptional repressor of muscle gene expression, and that miR-133 enhances myoblast proliferation by repressing serum response factor (SRF) [6], both examples of new molecular mechanisms to regulate skeletal muscle gene expression and embryonic developmental [6]. [score:9]
Overexpression of miRNA-1 in the mouse developing heart has a negative effect on muscle proliferation as it targets the transcription factor that promotes ventricular cardiomyocyte expansion, Hand2 [4]. [score:5]
In Drosophila, the expression of miR-1 is controlled by the Twist and Mef2 transcription factors [5]. [score:3]
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[+] score: 16
Muscle-specific miR-1-3p showed high expression levels in both libraries (LDM, 32.01%; PMM, 20.15%), and miRNAs that potentially affect metabolic pathways (such as the miR-133 and -23) showed significant differences between the two libraries, indicating that the two skeletal muscle types shared mainly muscle-specific miRNAs but expressed at distinct levels according to their metabolic needs. [score:5]
Our results are consistent with previous studies that found that miR-1, -133, and -206 frequently ranked among the highest expressed miRNAs in porcine muscle cell proliferation and differentiation [25, 40, 41]. [score:3]
In 2006, miR-1 and miR-206 were reported to regulate the myostatin gene which directly impacts muscular hypertrophy [14]. [score:3]
Muscle-specific miR-1 and -133 are transcriptionally regulated by myogenic differentiation factors (e. g., MyoD, Mef2, and SRF) [18], deletion of these miRNAs resulted in aberrant muscle maintenance. [score:2]
Both miR-1 and -181 promote mammalian myoblast differentiation and development [47], and it has been speculated that miR-1 plays a role in inducing antioxidant response in skeletal muscle [48]. [score:2]
Our finding that miR-1 accounted for 32.01% of the detected miRNAs in our LDM library is consistent with previous results. [score:1]
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[+] score: 16
However, as for the expression of miR-1 in BJ501-infected lung on 5 dpi, it was not significantly up-regulated from the results of microarray analysis while it down-regulated > 2-fold by RT-PCR analysis. [score:9]
We found that 86.11% (31 of 36) of the relative real-time RT-PCR results were consistent with those obtained in the microRNA microarray analysis in terms of direction of regulation at one or more time points except the results of miR-574-3p in BJ501-infected lung on 2 dpi, miR-1 in PR8-infected lung on 2 dpi, miR-1 in BJ501-infected lung on 5 dpi, miR-133a in PR8-infected lung on 2 dpi and miR-133b in PR8-infected lung on 2 dpi (Figure 5). [score:3]
There was no target for mmu-miR-1, mmu-miR-135a-1, mmu-miR-2145, mmu-miR-24-2 or mmu-miR-29b-1 in the database. [score:3]
Nine microRNAs (miR-1, miR-1187, miR-133a, miR-133b, miR-155, miR-2137, miR-223, miR-30d and miR-574-3p) were selected for validation. [score:1]
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[+] score: 15
In our study, prv-miR-1, prv-miR-3 and prv-miR-11 were predicted to target both LORF1 and LORF2, while prv-miR-2 and prv-miR-9 target LORF1, which reveal that there exist a similar self-regulation mechanism of PRV LLT and its miRNAs. [score:6]
Some miRNAs (like prv-miR-1 and prv-miR-3) can target multiple genes, while some genes (like LLT, IE180 and EP0) are targeted by multiple miRNAs. [score:5]
These viral miRNAs were designated as prv-miR-1 to prv-miR-11 (Figure 2B and Table 1). [score:1]
0030988.g004 Figure 4 (A) An example of terminal sequence variation of PRV miRNA prv-miR-1. Shown are the distribution and corresponding sequence reads of isomiRs. [score:1]
Four other pre-miRNAs (prv-miR-1, prv-miR-5, prv-miR-9 and prv-miR-11) and one mature miRNA, prv-miR-1-3′, were detected by northern blot as well (Figure 2F and Table 1). [score:1]
Of the above 17 detected viral miRNAs (Table 1), 4 miRNAs share the conserved but not completely identical sequences with those previously reported PRV miRNAs in DC, i. e., prv-miR-P1-3′ versus prv-miR-1, prv-miR-P5 versus prv-miR-3, prv-miR-P6-5′ versus prv-miR-2, and prv-miR-P9-5′ versus prv-miR-5 [10]. [score:1]
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[+] score: 12
Among 129 differentially expressed miRNAs in pig testes, 8 miRNAs including mmu-let-7e and mmu-miR-181b shared the same expression profile as the previous study in sexually immature/mature mouse testes [18], and 10 miRNAs including hsa-miR-1 and mmu-miR-709 had the same expression profile in the immature/mature rhesus monkey testes [19]. [score:7]
Such as the myostatin allele in muscle mass QTL interval is characterized by a G to A transition in the 3′ un-translated region (UTR) that creates a target site for miR-1 and miR-206 which are highly expressed in skeletal muscle. [score:5]
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[+] score: 12
Other miRNAs from this paper: ssc-mir-122, ssc-mir-214, ssc-mir-206, ssc-mir-10b
Interestingly, muscular hypertrophy in Texel sheep has been shown to be caused by a mutation that creates an illegitimate binding site for miR-1/206 in the 3' UTR of the myostatin gene, leading to efficient translational inhibition of the myostatin gene and an increase in muscularity [8]. [score:6]
The miR-1/206 showed high abundance of expression levels in muscle (Figure 3C). [score:3]
The miR-1 and miR-206 are key mediators in proper skeletal and cardiac muscle development and function, myogenesis during embryonic development and muscle cell differentiation [37]. [score:3]
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[+] score: 11
A number of miRNAs related to skeletal muscle growth and development were differentially expressed between low and high RFI pigs, including miR-208b, miR-499, miR-29c, miR-1 and miR-99b. [score:4]
Compared to RFI_H muscles, expression of miR-1 and miR-30e miRNAs was higher, whereas expression of miR-10b, and miR-145 was lower in RFI_L muscles (Fig. 1c). [score:4]
To validate the differential expression identified by the miRNA sequencing, miR-1, miR-30e, miR-10b and miR-145 were selected for qRT-PCR analysis. [score:3]
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[+] score: 10
For example, the miR-133 family (ssc-miR-133b, ssc-miR-133a-3p) as well as the let-7 family (ssc-miR-98, ssc-let-7e) was up-regulated in Bama minipigs; in the miR-1/206 family, ssc-miR-1 was up-regulated whilst ssc-miR-206 was down-regulated in Bama minipigs. [score:10]
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[+] score: 10
We have identified several miRNAs that are up-regulated in MSTN [-/-] pigs, and these miRNAs have previously been shown to be involved in myoblast development, including the well-known miR-1, miR-206 [13, 15], and miR-486 [26] (Figure 1A). [score:5]
Chen et al. [13– 15] previously reported that miR-1 and miR-206 can promote the differentiation of skeletal muscle satellite cells and significantly inhibit their proliferation by decreasing the expression level of Pax7. [score:5]
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23
[+] score: 9
The most up-regulated miRNA that was expressed in the pituitary relative to skeletal muscle was miR-222, and miR-1 was the most down-regulated. [score:9]
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[+] score: 9
Ssc-miR-1 and ssc-miR-133 were also highly expressed and ranked the 4 [th] and 28 [th] respectively. [score:3]
Hou et al. [40] showed that ssc-miR-206, ssc-miR-378, and ssc-miR-1 were expressed at extremely high levels in the longissimus dorsi muscles of Tong Cheng pigs. [score:3]
For example, muscle-specific miRNAs (myomiRs), such as miR-1, miR-133a/b, miR-206, and miR-486, were shown to be involved in the regulation of skeletal muscle hypertrophy by modulating the IGF-1–Akt pathway and myostatin signaling pathway [13– 17]. [score:2]
In the present study, we found that ssc-miR-206, ssc-miR-378, and ssc-miR-1 were ranked 1 [st], 3 [rd], and 4 [th] in abundance among the ten libraries, which is consistent with the previous study. [score:1]
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25
[+] score: 7
Koutsoulidou A Mastroyiannopoulos NP Furling D Uney JB Phylactou LA Expression of miR-1, miR-133a, miR-133b and miR-206 increases during development of human skeletal muscleBMC Dev. [score:4]
Interestingly, the expression patterns of myogenic miRNAs (miR-1, 206 and 133) also showed distinct between-breed differences in G1 and G2. [score:3]
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[+] score: 7
Notably, prv-miR-1, prv-miR-14a, prv-miR-17a, prv-miR-21, prv-miR-24 and prv-miR-25 were encoded directly antisense to the individually corresponding coding gene, which could theoretically lead to the cleavage of the transcript and negative regulation of the gene. [score:3]
Among 25 mature viral miRNAs, 20 miRNAs expressed in PRV JS-2012-infected PK15 cells were detected using this approach, with the exception of prv-miR-1, 6, 16, 21 and 25 (Fig 2). [score:3]
Twenty of them were confirmed through stem-loop RT-qPCR excepted prv-miR-1, 6, 16, 21 and 25 (Fig 2). [score:1]
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[+] score: 6
Shown are the unique sequences and number of times this sequence was detected matching the pre-miRNA sequence of ssc-miR-1. The most frequent occurring miR-1 sequence is in accordance with the miRBase reference sequence. [score:1]
For example, porcine F37976_x4, F1_x405541, and F500_x373 from the Solexa sequences matched dya-miR-1, ptr-miR-1, and rno-miR-1, respectively. [score:1]
An example is given in Figure 3, demonstrating sequenced isomiRs for miR-1, which indicated that the majority of porcine miRNA nucleotide variants resulted from post-transcriptional modifications. [score:1]
These three miRNAs have sequence differences, so F37976_x4, F1_x405541, and F500_x373 may be isomiR of miR-1 in the pig. [score:1]
0016235.g003 Figure 3 Shown are the unique sequences and number of times this sequence was detected matching the pre-miRNA sequence of ssc-miR-1. The most frequent occurring miR-1 sequence is in accordance with the miRBase reference sequence. [score:1]
An example of a miR-1 isomiR not matching the genome is shown in the italic part of the figure. [score:1]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
For example, miR-273 and the lys-6 miRNA have been shown to be involved in the development of the nervous system in nematode worm [3]; miR-430 was reported to regulate the brain development of zebrafish [4]; miR-181 controlled the differentiation of mammalian blood cell to B cells [5]; miR-375 regulated mammalian islet cell growth and insulin secretion [6]; miR-143 played a role in adipocyte differentiation [7]; miR-196 was found to be involved in the formation of mammalian limbs [8]; and miR-1 was implicated in cardiac development [9]. [score:6]
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[+] score: 6
Many miRNAs, such as miR-1, miR-133, miR-29, miR-214, miR-206, miR-486, miR-208b, and miR-499 were involved in the regulation of skeletal myogenesis by binding to its target genes 36, 37. [score:4]
For example, in mice, miR-1 and miR-133 are clustered on the same chromosomal loci and transcribed together in a tissue-specific manner during development, but miR-133 enhances proliferation by repressing serum response factor, whereas miR-1 promotes myogenesis through repressing histone deacetylase 4 [19]. [score:2]
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[+] score: 6
Other miRNAs from this paper: ssc-mir-206
The importance of MYOD1 in regulating the apoptosis of myoblasts via inducing the expression of miR-1 and miR-206 has been demonstrated [35, 36]. [score:4]
Chen J. Tao Y. Li J. Deng Z. Yan Z. Xiao X. Wang D. microRNA-1 and microRNA-206 regulate skeletal muscle satellite cell proliferation and differentiation by repressing Pax7 J. Cell Biol. [score:2]
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[+] score: 5
Other miRNAs from this paper: ssc-mir-206
The myostatin (MSTN) allele of Texel sheep was characterized by a G to A transition in the 3′UTR that created a target site for miR-1 and miR-206, which caused the translational inhibition of the MSTN gene and contributed to the muscular hypertrophy of Texel sheep 33. [score:5]
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32
[+] score: 5
A similar demonstration of paramutation in mice was achieved by microinjecting microRNA miR-1 in fertilized oocytes to target the Cdk9 cardiac growth regulator [12]. [score:5]
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33
[+] score: 5
Three miRNAs appeared twice among them, thus a total of 14 miRNAs (ssc-miR-1, -21, -133b, -144, -145-5p, -146a-5p, -146b, -183, -196b-5p, -206, -224, -365-3p, -370, and -4334-3p) were detected to differentially express in response to 1.5% CLA treatment (Table 2, Figure 2, and Table S9). [score:3]
Among another 12 DE miRNAs, three miRNAs (miR-1, -133b, and -206) are defined as myogenic miRNAs [35, 36]. [score:1]
Six DE miRNAs (ssc-miR-1, -21, 145-5p, -146b, -146a-5p, and -206) were selected for qPCR to validate the RNA sequencing results. [score:1]
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[+] score: 5
McCarthy J. J. Esser K. A. MicroRNA-1 and microRNA-133a expression are decreased during skeletal muscle hypertrophy J. Appl. [score:3]
In contrast, miR-1, miR-133a/b and miR-206, as muscle-specific miRNAs, were not the most abundant miRNAs in our data. [score:1]
Previous studies have demonstrated that the myomiRs miR-1, miR-133a/b, miR-206, miR-486, miR-26a, miR-27b, miR-378, miR-148a and miR-181 are highly enriched in skeletal muscle and play a key role in skeletal muscle metabolism [28, 29, 30, 31]. [score:1]
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[+] score: 5
It post-transcriptionally represses the expression of genes in antioxidant network and thus influences susceptibility to cardiac oxidative stress of miR-1 transgenic mice [68]. [score:3]
MiR-1 family is abundantly expressed in cardiac and skeletal muscle. [score:2]
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36
[+] score: 4
The muscle specifically expressed or highly enriched miRNAs, such as miR-1, miR-133, miR-206 and miR-208, which are responsible for the transcriptional networks involving SRF, MyoD, MEF2 and myocardin, and play central regulatory roles in myoblast proliferation and differentiation during myogenesis [8, 9, 10]. [score:4]
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[+] score: 4
MiR-208b-3p, miR-1, miR-16 and miR-195 were upregulated with a fold change of > 1.5 and p value < 0.05. [score:4]
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[+] score: 4
Other miRNAs from this paper: ssc-mir-133a-1, ssc-mir-133a-2
Additionally, sildenafil treatment inhibited the increases in the microRNA-1 levels and alleviated the decreases in the microRNA-133a levels which negatively regulate pro-apoptotic genes [48]. [score:4]
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[+] score: 3
In addition, miR-1 and miR-133 had highest levels of expression in the heart, miR-181a and miR-142-3p in the thymus, miR-194 in the liver, and miR-143 in the stomach. [score:3]
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40
[+] score: 3
West Nile virus (WNV)-encoded KUN-miR-1 facilitates virus replication [23], while a dengue virus (DENV)-encoded vsRNA inhibits viral replication [24]. [score:3]
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41
[+] score: 3
12946) miR-16-5p Potential regulator of SMAD3 102 1.23E-24 −9.938 Li et al. 2015 (10.2174/1381612821666150909094712) miR-1-3p Unknown 99 5.58E-24 −9.767 n/a let-7a-5p Potential regulator of CCND1 and MYC 78 7.77E-20 −8.622 Ghanbari et al. 2015 (10.4137/BIC. [score:3]
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[+] score: 2
h CAAAUGC ssc-miR-19b 1.50 miR-19 GUGCAAA ssc-miR-183 1.47 miR-183 AUGGCAC ssc-miR-423-3p 1.46 miR-423/423-3p GCUCGGU ssc-miR-206 1.46 miR-1/206 GGAAUGU ssc-miR-15a 1.42 miR-15/16/195/424/497 AGCAGCA ssc-miR-22-5p 1.39 miR-22-5p/3568 GUUCUUC ssc-miR-133a-3p 1.39 miR-133 UUGGUCC ssc-miR-340 1.37 miR-340/340-5p UAUAAAG ssc-let-7a 1.37 let-7/98 GAGGUAG ssc-miR-338 1.36 miR-338/338-3p CCAGCAU ssc-miR-361-5p 1.35 miR-361/361-5p UAUCAGA 10.1371/journal. [score:1]
h CAAAUGC ssc-miR-19b 1.50 miR-19 GUGCAAA ssc-miR-183 1.47 miR-183 AUGGCAC ssc-miR-423-3p 1.46 miR-423/423-3p GCUCGGU ssc-miR-206 1.46 miR-1/206 GGAAUGU ssc-miR-15a 1.42 miR-15/16/195/424/497 AGCAGCA ssc-miR-22-5p 1.39 miR-22-5p/3568 GUUCUUC ssc-miR-133a-3p 1.39 miR-133 UUGGUCC ssc-miR-340 1.37 miR-340/340-5p UAUAAAG ssc-let-7a 1.37 let-7/98 GAGGUAG ssc-miR-338 1.36 miR-338/338-3p CCAGCAU ssc-miR-361-5p 1.35 miR-361/361-5p UAUCAGA 10.1371/journal. [score:1]
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[+] score: 2
The five most abundant miRNAs represented 47.9% of the total cpm in the dataset including ssc-miR-1, ssc-miR-133a­3p, ssc­miR-378, ssc-miR-206, and ssc-miR-10b. [score:1]
These miRNAs have previously been identified in pig skeletal muscle, including Nielsen et al. [11], where ssc-miR-1 and ssc-miR-206 were the two most highly abundant miRNAs identified from sequencing LD samples from seven 1.5–2-year-old Danish Landrace/Yorkshire crossbred pigs. [score:1]
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[+] score: 1
For example, in the Texel sheep, the creation of miR-1 and miR-206 binding sites by a SNP in the 3′ UTR region of the GDF8 shows perfect association with sheep hyper-muscularity [20], [21]. [score:1]
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[+] score: 1
The genomic locations of these five miRNAs (prv-miR-1 to prv-miR-5) indicated that they are transcribed as part of the intronic region of the Large Latency Transcript (LLT), more precisely from positions 97929 to 100397 of the viral genome. [score:1]
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[+] score: 1
Abbreviations: CECs = circulating endothelial cells, other abbreviations as in Fig 3. Studies have found that elevated miRNAs during ACS come from several origins: skeletal muscle miRNAs (miR-1 [8], -133a [9], and -133b), cardiac-specific miRNAs (miR-208a [9], -208b, -499, and -499-5p [8]), pancreatic miRNAs (miR-375), liver-specific miRNAs (miR-122), brain-enriched miRNAs (miR-34a, -124, -134, and -134-5p [10]) [8– 10], and endothelium-enriched miRNAs (miR-221-3p [11], -126, and -423 [12]). [score:1]
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[+] score: 1
Chen J. F. Man del E. M. Thomson J. M. Wu Q. Callis T. E. Hammond S. M. Conlon F. L. Wang D. Z. The role of microRNA-1 and microRNA-133 in skeletal muscle proliferation and differentiationNat. [score:1]
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