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13 publications mentioning gga-mir-140

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-140. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 176
A previous study showed that miR-140-3p was immediately down-regulated in skeletal muscle within one hour of refeeding after fasting for one week [33], and target prediction and expressional analyses suggested that miR-140-3p might bind and inhibit the expression of the myostatin gene, which is a well-known negative regulator of muscle growth [34, 35, 36]. [score:13]
However, MyHC expression significantly decreased (Figure 6F), suggesting that Myomaker is not the only target of miR-140-3p that regulated myoblast fusion and differentiation, and that there is another target gene for miR-140-3p that can regulate MyHC expression and myoblast fusion. [score:11]
Altogether, in an in vitro system, miR-140-3p can inhibit Myomaker expression by binding directly to the 3ʹ UTR of Myomaker mRNA and can regulate myoblast cell cycle progression and differentiation by other target genes. [score:9]
It is possible that there are other target genes of miR-140-3p that can regulate MyHC expression, because Myomaker loss-of-function has no impact on MyHC expression. [score:8]
Finally, to understand the post-transcriptional regulation of Myomaker expression, we analysed the 3ʹ UTR of Myomaker and found that miR-140-3p can inhibit Myomaker expression by binding to the Myomaker 3ʹ UTR in vitro. [score:8]
Co-transfection of miR-140-3p with a Myomaker 3ʹ UTR dual-luciferase construct repressed luciferase activity significantly, and the mutation of each of the two target sites in the 3ʹ UTR relieved this repression (Figure 6H), indicating that miR-140-3p can directly bind to either of these two target sites in the Myomaker 3ʹ UTR. [score:7]
In our results, miR-140-3p overexpression inhibited Myomaker and MyHC expression. [score:7]
Importantly, this study is the first to demonstrate that miR-140-3p can target inhibit Myomaker expression during myoblast differentiation. [score:7]
2.6. miR-140-3p Binds Directly to the 3ʹ UTR of Myomaker and Inhibits Myomaker Expression in Vitro. [score:6]
Karlsen T. A. Jakobsen R. B. Mikkelsen T. S. Brinchmann J. E. microRNA-140 targets RALA and regulates chondrogenic differentiation of human mesenchymal stem cells by translational enhancement of SOX9 and ACAN Stem Cells Dev. [score:6]
Among these miRNAs (Supplementary File 1), we found that miR-140-3p, which has two potential binding sites in Myomaker mRNA 3ʹ UTR (Figure 6A), can significantly inhibit Myomaker mRNA expression in primary myoblast (Figure 6B). [score:5]
Additionally, miR-140-3p overexpression did not alter the expression of MYOG and MYOD (Figure 6F). [score:5]
Therefore, these results not only demonstrate that Myomaker regulates avian myoblast fusion, but also that three regulators, MYOD, MYOG and miR-140-3p, can influence Myomaker expression during myoblast differentiation. [score:5]
miR-140-3p overexpression inhibited the late stage of myoblast differentiation but promoted myoblast proliferation. [score:5]
However, the mechanism of miR-140-3p inhibited MyHC expression remains unclear. [score:5]
Moreover, we found for the first time that miR-140-3p can inhibit Myomaker expression and myoblast fusion, at least in part, by binding to the 3ʹ UTR of Myomaker. [score:5]
Additionally, miR-140-3p overexpression during myoblast fusion inhibited cell fusion and led to smaller myotubes with less nuclei than the cells of the control (Figure 6C,D). [score:5]
Jude J. A. Dileepan M. Subramanian S. Solway J. Panettieri R. J. Walseth T. F. Kannan M. S. miR-140-3p regulation of TNFα -induced CD38 expression in human airway smooth muscle cells Am. [score:4]
Collectively, our results confirmed the important roles of Myomaker in avian myoblast fusion and found that MYOD, MYOG and miR-140-3p could regulate Myomaker expression. [score:4]
Because cell cycle arrest is important for myoblast differentiation, we next analysed whether miR-140-3p overexpression could regulate the cell cycle of myoblasts in vitro. [score:4]
However, the roles and expression pattern of miR-140-3p are similar to those of miR-133a, which is an important muscle-specific miRNA during muscle development [42, 43, 44]. [score:4]
The Myomaker gene is a direct target of miR-140-3p. [score:4]
Luciferase activity was determined at 36 h after transfection; (I) miR-140-3p expression during myoblast differentiation; (J) Cell cycle analysis of myoblasts at 36 h after miR-140-3p mimic or NC duplexes transfection. [score:3]
The 3ʹ UTR of Myomaker mRNA has two predicted target sites for miR-140-3p (Figure 6G). [score:3]
To our surprise, miR-140-3p expression gradually increased during the differentiation process (Figure 6I). [score:3]
However, the regulatory mechanism of miR-140-3p during myoblast differentiation remains unclear, and its regulatory role in Myomaker is limited to the in vitro system. [score:3]
Therefore, miR-140-3p may be a positive regulator during muscle development similar to miR-133a. [score:3]
Additionally, miR-140-3p expression during myoblast differentiation is consistent with Myomaker, suggesting that this miRNA may have another function in this process. [score:3]
This expression pattern was similar to those of Myomaker, MYOG and MYOD, suggesting that miR-140-3p may have another important function during myoblast differentiation. [score:3]
miR-140-3p can also regulate the cell cycle of myoblasts. [score:2]
However, few studies have examined miR-140-3p involvement in muscle development. [score:2]
Cell cycle analysis revealed that miR-140-3p transfected cells showed a lower percentage of G1 and G2 phase entries and a significantly higher percentage of S phase entry than cells transfected with control (Figure 6J and Supplementary File 2), demonstrating that miR-140-3p can regulate myoblast cell cycle progression in vitro. [score:2]
For miRNA target validation assays, wild-type or mutant Myomaker 3ʹ UTR dual-luciferase reporter (100 ng) and miR-140-3p mimic or NC duplexes (50 nM) were co -transfected into DF-1 cells using the Lipofectamine 3000 reagent (Invitrogen, Carlsbad, CA, USA) in 96-well plates. [score:2]
Another study in human airway smooth muscle cells showed that miR-140-3p attenuates the activation of NF-κB and p38 MAPK by indirect mechanisms [37]. [score:2]
The fusion index of miR-140-3p transfected cells significantly decreased (Figure 6E). [score:1]
The specific function and mechanism of miR-140-3p in myoblast differentiation and proliferation remains to be further explored. [score:1]
The mutant Myomaker-3ʹ UTR reporters were generated by changing the miR-140-3p binding site from CCTGTG to TTCACA, and mutagenesis was carried out by PCR amplification and DpnI digestion to remove the parental DNA. [score:1]
Here, we found that the miRNA miR-140-3p is another candidate involved in myoblast fusion in vitro. [score:1]
Therefore, the function of miR-140-3p in muscle remains to be explored. [score:1]
Zou M. X. Huang W. Wang X. B. Lv G. H. Li J. Deng Y. W. Identification of miR-140-3p as a marker associated with poor prognosis in spinal chordoma Int. [score:1]
Cell cycle arrest is an important event for myoblast differentiation, and our results showed that miR-140-3p promotes myoblast proliferation, suggesting the negative role of miR-140-3p in myoblast differentiation. [score:1]
miR-140-3p can play roles in chondrogenic differentiation [30], testis differentiation [31] and spinal chordoma prognosis [32]. [score:1]
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[+] score: 29
Target genes of gga-miR-199* and gga-miR-140*, for which whose seed sequences could not be found in TargetScan, were predicted by TargetScanHuman Custom (Version 5.3). [score:7]
Six miRNAs (gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-222, gga-miR-199*, and gga-miR-140*) were down-regulated and one miRNA (miR-146c) was up-regulated in MDV-infected samples, and especially in MD lymphomas, compared to non-infected samples. [score:6]
gga-miR-181a, gga-miR-26a, gga-miR-221, gga-miR-199*, and gga-miR-140* were down-regulated (Figure 2A–E). [score:4]
Its significant down-regulation in the current study strongly implicates involvement of miR-140* in oncogenic transformation. [score:4]
F. Expression of gga-miR-140* among TS, LL, and NS. [score:3]
Differential expression of miR-199* and miR-140* in MDV-infected samples was reported here for the first time. [score:3]
Three 3p-derived miRNAs (gga-miR-199-3p, gga-miR-22-3p, and gga-miR-140-3p) had more counts than their corresponding 5p-derived miRNAs. [score:1]
To our knowledge, this is the first report of involvement of miR-140* in tumors. [score:1]
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[+] score: 27
Comparing the inhibition of luciferase activity by the lentiviral expressed and endogenously expressed miRNAs, these results show that 1) the lentiviral expressed miR126 (both sense and antisense strands) and miR140 antisense strand exhibit potent RNAi activity; 2) the lentiviral expressed miR451 antisense strand does not have any RNAi activity; 3) the observed RNAi activity of lentiviral expressed miR21 (both sense and antisense strands) and miR140 sense strand could be due to endogenous miRNAs. [score:13]
Expression of both the sense and antisense strands of gga-miR21, gga-miR126 and gga-miR140 led to the inhibition of Renilla luciferase activity (Figure 2a). [score:5]
Based on literature reports and the miRNA database (miRBase), we chose four endogenous chicken miRNAs gga-miR21, gga-miR126, gga-miR140 and gga-miR451 that are expressed in many different tissues of adult chicken and chicken embryo [22]. [score:3]
As shown in Figure 2b, Renilla luciferase activity was inhibited by ∼98% by the sense strand of gga-miR21, ∼20% by the antisense strand of gga-miR21, and ∼60% by the sense strand of gga-miR140. [score:3]
Because gga-miR21, gga-miR126, gga-miR140 and gga-miR451 are generally expressed, we assayed their activity in DF-1 cells by directly transfecting the reporter plasmids into DF-1 cells. [score:3]
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[+] score: 14
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-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-140, hsa-mir-125b-2, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-367, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-125b-2, gga-mir-155, gga-mir-222a, gga-mir-221, gga-mir-92-1, gga-mir-19b, gga-mir-20a, gga-mir-19a, gga-mir-18a, gga-mir-17, gga-mir-16-1, gga-mir-15a, gga-mir-1a-2, gga-mir-206, gga-mir-223, gga-mir-106, gga-mir-302a, gga-mir-181a-1, gga-mir-181b-1, gga-mir-16-2, gga-mir-15b, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-146a, gga-mir-181b-2, gga-mir-181a-2, gga-mir-1a-1, gga-mir-1b, gga-let-7a-2, gga-mir-34b, gga-mir-34c, gga-let-7j, gga-let-7k, gga-mir-23b, gga-mir-27b, gga-mir-24, gga-mir-122-1, gga-mir-122-2, hsa-mir-429, hsa-mir-449a, hsa-mir-146b, hsa-mir-507, hsa-mir-455, hsa-mir-92b, hsa-mir-449b, gga-mir-146b, gga-mir-302b, gga-mir-302c, gga-mir-302d, gga-mir-455, gga-mir-367, gga-mir-429, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-1458, gga-mir-1576, gga-mir-1612, gga-mir-1636, gga-mir-449c, gga-mir-1711, gga-mir-1729, gga-mir-1798, gga-mir-122b, gga-mir-1811, gga-mir-146c, gga-mir-15c, gga-mir-449b, gga-mir-222b, gga-mir-92-2, gga-mir-125b-1, gga-mir-449d, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-122b-2
MiR-1a, miR-140 and miR-449 were significantly up-regulated in both tissues, while miR-455, miR-34b and miR-34c were only up-regulated with AIV infection in tracheae. [score:7]
Of particular interest, miR-1a, miR-140, and miR-449, which were highly expressed in infected tracheas than the non-infected ones, and also were differentially expressed between infected tissues (higher expression levels in infected tracheae than infected lungs). [score:7]
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[+] score: 8
Co-transfection of a BAF60a sensor with miR-133 led to downregulation of luciferase expression compared with co-transfection with miR-140, an unrelated miRNA not predicted to target the 3′UTR. [score:7]
pGL3 vector without 3′UTR or with mutant 3′UTRs, or the transfection of unrelated miR-140, served as a negative control. [score:1]
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[+] score: 7
In this analysis, only the 18 most abundant miRNAs (excluding the let-1 family, which is ubiquitously expressed, but including miR-140) were used for target gene prediction and a total of 1253 genes were detected and then subjected for KEGG Orthology analysis (Additional file 10: Table S8). [score:5]
The involvement of mmu-miR-199a and miR-140 in hair follicle and skin development are related to hair follicle cycling in mammals [24, 43]. [score:2]
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[+] score: 6
Of these miRNAs, miR-6548-5p, miR-6631-5p, miR-92-5p and miR-140-3p potentially regulated of 15, 9, 7 and 7 mRNA respectively. [score:2]
Moreover, in the E11_VS_P1 contrast group, eleven miRNAs (miR-6548-5p, miR-19a-5p, miR-3536, miR-6631-5p, miR-222a, miR-140-3p, miR-92-5p, miR-135a-5p, miR-455-3p, miR-460a-5p and miR-200a-3p), were highly regulated. [score:2]
In E11_VS_P1, miR-6548-5p, miR-6631-5p, miR-92-5p and miR-140-3p were regulators. [score:2]
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[+] score: 5
Reduced miR-140 expression was observed in human OA cartilage [53, 54]. [score:3]
MiR-140 plays dual roles in both cartilage development and homeostasis, in part via by regulating Adamts-5 in OA [55]. [score:2]
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[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Out of the 26 miRNA/host gene pairs with coordinated expression, 11 have been found to be coordinately expressed in both, human and mouse [19], [27], [59], [61]– [64], [67]– [69], [71], [73]– [79]: mir-103/ PANK3, mir-107/ PANK1, mir-126/ EGFL7, mir-128-1/ R3HDM1, mir-140/ WWP2, mir-211/ TRPM1, mir-218-1/ SLIT2, mir-218-2/ SLIT3, mir-27b/ C9orf3, mir-33/ SREBF2, and mir-499/ MYH7B. [score:5]
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[+] score: 3
The regulatory effect of miR-4510, miR-4460, miR-135b-3p, miR-4635, miR-4252, miR-376b-3p, miR-140-5p and miR-548aa on membrane GPC3 levels was confirmed (Figure 2B). [score:2]
MiR-4460 was not detected in liver, whereas miR-135b-3p, miR-4635, miR-4252 and miR-140-5p were not deregulated in tumors compared to NTL (Supplementary Figure 3A-3B). [score:1]
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[+] score: 2
One striking exception to this general trend was gga-miR-140*; this was present as 911 reads in the layers and 711 reads in the broilers libraries, but gga-miR-140 was not detected in either library (Table 2), suggesting that gga-miR-140* functions during chicken skeletal muscle development. [score:2]
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[+] score: 1
One intriguing exception was gga-miR-140*, which was present as 105,474 reads in the mature ovary and 95,992 reads in the immature ovary; however, gga-miR-140 had only 7,370 and 7,953 reads in each library, respectively. [score:1]
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[+] score: 1
Of these, nine (gga-mir-1b, gga-mir-7, gga-mir-7b, gga-mir-10b, gga-mir-31, gga-mir-130b, gga-mir-204, gga-mir-215, gga-mir-489) are increased, and five (gga-mir-223, gga-mir-124b, gga-mir-140, gga-mir-183, gga-mir-222a) are decreased in CD30 [hi] cells. [score:1]
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