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16 publications mentioning gga-mir-203b

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-203b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 400
More importantly, miR-203 overexpression at different myoblast differentiation stages significantly inhibited the MEF2C protein level but not the MEF2C mRNA level (Figure 7f), and the expression levels of three muscle-specific genes, MYOM1 (myomesin 1), MYOM2 (myomesin 2) and MCK (muscle creatine kinase), which are directly regulated by MEF2C, [15] were all significantly downregulated (Figure 7f). [score:12]
The protein expression of MEF2C was downregulated during E14 and E16 (Figure 7a), and it was upregulated from proliferation to differentiation of myoblasts (Figure 7b), demonstrating that MEF2C expression correlated with miR-203 levels in vitro and in vivo. [score:11]
The expression of miR-203 is upregulated in proliferating myoblasts and is sharply downregulated during differentiation in vitroTo further study the potential roles of miR-203, we separated chicken primary myoblasts (Figure 2a) and observed the expression profiles of miR-203 in vitro. [score:11]
Together with the miR-203 expression data, we found that higher or upregulated expression of miR-203 is accompanied by slow leg muscle development, and the low expression of miR-203 is followed by a rapid increase in muscle weight and full formation of muscle fibres. [score:11]
Both p53 and p21 expressions were significantly downregulated or upregulated with miR-203 overexpression or loss-of-function, respectively (Figures 5g and h). [score:11]
During dwarf chicken leg muscle development, miR-203 exhibits transient upregulated expression from E10–E16 but is sharply downregulated after E16. [score:10]
More importantly, the transfection of myoblasts with miR-203 in GM downregulated c-JUN mRNA and protein expression (Figure 5c), and the inhibition of endogenous miR-203 in GM using anti-miR-203 increased c-JUN mRNA and protein expression (Figure 5d). [score:10]
[33] Furthermore, during skeletal muscle development in dwarf chickens, miR-203 expression is upregulated from E10–E16 and sharply downregulated after E16 (Figure 1e). [score:10]
The expression of miR-203 is upregulated in proliferating myoblasts and is sharply downregulated during differentiation in vitro. [score:9]
In normal chickens, miR-203 is highly expressed at E12 and E14, and miR-203 expression is sharply downregulated after E18 (Supplementary File 1). [score:8]
Under this condition, the expression of myogenin was significantly downregulated, and the expression of MHC was slightly lower in the miR-203 -transfected myoblasts than that in the control myoblasts (Figure 4b). [score:8]
Knockdown of MEF2C expression mimicked the overexpression of miR-203 by inhibiting the differentiation of myoblasts. [score:8]
c-JUN is a direct target of miR-203 in chickensc-JUN is a positive regulator of cell proliferation, 20, 21 and c-JUN is a direct target of miR-203 in basal cell carcinoma. [score:8]
These results indicated that miR-203 is expressed in proliferating chicken primary myoblasts, but such expression is sharply downregulated during myoblast differentiation. [score:8]
MEF2C is a direct target gene of miR-203 that has a positive role in myoblast differentiation c-JUN is a direct target of miR-203; however, no study has reported its relationship with myogenic differentiation. [score:7]
The results showed that a significant increase in myogenin and MHC expression, as well as the fusion index, was observed, when miR-203 expression was inhibited (Figures 4g–i). [score:7]
27, 30, 42, 43, 44, 45, 46 We found here that miR-203 can also inhibit myoblast proliferation by repressing c-JUN expression, an established target of miR-203 in human basal cell carcinoma. [score:7]
In addition, one consequence of MEF2C activation is to increase the transcription of c-JUN in C2C12 cells and inflammatory cells, 54, 55 and the overexpression of c-JUN suppresses miR-203 expression. [score:7]
[35] In addition, p63, another target of miR-203 in skin differentiation and in RMS cells, 28, 29, 30, 47 was inhibited in miR-203 -overexpressed myoblasts (Supplementary File 9). [score:7]
Because the inhibition of cell proliferation by c-JUN is p53 dependent, [21] we also detected the expression of p53 and p21 in miR-203 overexpression and loss-of-function myoblasts and control myoblasts. [score:7]
In addition, subsequent miR-203 overexpression results showed that miR-203 can significantly inhibit myoblast proliferation and differentiation by repressing c-JUN and MEF2C expression. [score:7]
miR-203 was expressed in undifferentiated primary myoblasts at both subconfluence (50% growth medium (GM)) and full confluence (100% GM; Figures 2c and d) but was sharply downregulated when cells underwent differentiation, as indicated by the appearance of myogenin transcripts (Figure 2b). [score:6]
To determine whether miR-203 can directly target c-JUN, we constructed two dual-luciferase reporters with the wild-type or mutant 3'-untranslated regions (3'-UTRs) of c-JUN inserted at the 3' end of the firefly luciferase gene (Figure 5e). [score:6]
MEF2C, a new target of miR-203 found in this study, is upregulated during C2C12 differentiation, [53] and its interaction with MAML1, Notch3 and the p38 MAPK pathway is required for normal myogenesis (Figure 8). [score:6]
[50] The downregulated expression of miR-203 from myoblast proliferation to differentiation is similar to that observed for miR-155, miR-125, miR-669a and miR-669q, 2, 51, 52 which all act to repress skeletal muscle differentiation. [score:6]
[53] In our study, the MEF2C protein level was also upregulated during myoblast differentiation, and the overexpression of miR-203 repressed the MEF2C protein level and myoblast differentiation. [score:6]
These results indicated that the predicted site is a target of miR-203 and is responsible for miR-203 targeting of the c-JUN 3'-UTR. [score:5]
The expression of c-JUN and MEF2C correlated well with miR-203 expression during myoblast differentiation. [score:5]
In RMS cells, re -expression of miR-203 can induce myogenic differentiation by targeting p63 and LIFR. [score:5]
miR-203 is wi dely recognised as an inhibitor of proliferation in various cancer lines by repressing various target genes. [score:5]
Collectively, miR-203 inhibits myoblast proliferation, in part, by repressing c-JUN expression. [score:5]
39, 40 In our study, miR-203 is transiently upregulated at E10–E16 in chicken embryo leg muscle but is not detected after birth, indicating its potential role in muscle development. [score:5]
Considering that miR-203 is specifically expressed in the skin, its high expression level in embryonic leg muscle can be due to the pollution of skin tissue. [score:5]
c-JUN is a positive regulator of cell proliferation, 20, 21 and c-JUN is a direct target of miR-203 in basal cell carcinoma. [score:5]
Northern blot analysis showed that miR-203 is indeed expressed in the leg muscle of E14 chickens but is not expressed in the leg muscle of 7-wk-old chickens (Figure 1b). [score:5]
MEF2C is a direct target gene of miR-203 that has a positive role in myoblast differentiation. [score:4]
These findings suggested that miR-203 might have an inhibitory role in skeletal muscle development. [score:4]
[34] To better understand the potential role of miR-203, we next studied the skeletal muscle phenotypes during chicken embryonic development and observed their correlation with miR-203 expression. [score:4]
In conclusion, the embryonic expression pattern of miR-203 during skeletal muscle development in chickens is transient, and another important role of miR-203 is to repress muscle proliferation and differentiation. [score:4]
c-JUN is a direct target of miR-203; however, no study has reported its relationship with myogenic differentiation. [score:4]
Altogether, these results confirmed that miR-203 is expressed in chicken embryonic skeletal muscle and indicated that it might have potential roles in skeletal muscle development. [score:4]
The high expression level of miR-203 at E14 and E16 was also validated using Northern blot (Figure 1f), although the low expression of miR-203 could not be detected at other stages due to the low sensitivity of the assay. [score:4]
Therefore, we argued that c-JUN is a direct target of miR-203 in chickens. [score:4]
c-JUN is a direct target of miR-203 in chickens. [score:4]
miR-203 expression correlates with chicken embryonic skeletal muscle development. [score:4]
Conversely, c-JUN knockdown significantly reduced myoblast proliferation (Figure 6e) and increased cell cycle arrest in the G0/G1 stage (Figure 6f and Supplementary File 7), a finding that is very similar to the effect of miR-203 overexpression. [score:4]
In the present study, we demonstrated a transient expression pattern of miR-203 during embryonic skeletal muscle development and presented a role for miR-203 in myoblast proliferation and differentiation (Figure 8). [score:4]
Thus, MEF2C is a target of miR-203, and its knockdown significantly represses the late stage of myoblast differentiation. [score:4]
Another study also detected miR-203 expression in chicken embryo skeletal muscle. [score:3]
miR-203 inhibits cell proliferation and induces cell cycle arrest in myoblasts. [score:3]
Although the predicted miR-203 targeting sequence in the chicken 3'-UTR of c-JUN has one mismatch in the seed region (Figure 5e, bottom), the sequence also has two additional potential base pairings with miR-203 outside of the 7-mer seed region. [score:3]
[49] According to our results, overexpression of miR-203 supressed myoblast differentiation, suggesting that the role of miR-203 may be different between RMS cells and myoblast. [score:3]
25, 41 miR-203 was shown to exhibit higher expression in E14 dwarf chickens and in layers than in E14 normal chickens and in broilers. [score:3]
Myogenin and MHC were both significantly downregulated in the miR-203 -transfected myoblasts compared with the control myoblasts (Figure 4c). [score:3]
To further study the potential roles of miR-203, we separated chicken primary myoblasts (Figure 2a) and observed the expression profiles of miR-203 in vitro. [score:3]
Therefore, we argued that there may be another target of miR-203 that functions in myogenic differentiation. [score:3]
29, 47, 48 Its knockdown represses myogenic differentiation, [49] suggesting another possible regulation pathway of miR-203 in myoblast proliferation and differentiation. [score:3]
In addition, the fusion index of the miR-203 -transfected myoblasts showed that miR-203 can significantly inhibit myoblast fusion (Figure 4f). [score:3]
In addition, miR-203 loss-of-function increased MEF2C protein level but not mRNA level, and the three genes were all upregulated as compared with controls (Figure 7g). [score:3]
Our previous microarray data showed that the expression level of miR-203 is significantly higher in the leg muscle of embryonic day 14 (E14) dwarf chickens than in E14 normal chickens (Figure 1a). [score:3]
[35] Here, we studied the involvement of c-JUN in the inhibition of miR-203 during myoblast proliferation. [score:3]
However, there were no differences in the expression levels of the cells transfected with the miR-203 and those transfected with the control duplex (Figure 4a). [score:3]
[36] However, in the current study and our previous data, [33] we found that miR-203 is abundantly expressed at E14 and E16 in chicken skeletal muscle. [score:3]
The latter correlation was further validated using a series of in vitro miR-203 overexpression, loss-of-function and functional testing experiments. [score:3]
In addition, the expression level of miR-203 in 100% GM was a little higher than that in 50% GM (Figures 2c and d). [score:3]
[33] Surprisingly, miR-203 shows abundant detection signals at E14 in both types of chickens but is not expressed at the age of 7 weeks (7 wk; Figure 1a). [score:3]
Together, these results showed that c-JUN can promote myoblast proliferation and this role is one reason for the inhibition of myoblast proliferation by miR-203. [score:3]
Together, we argued that miR-203 can inhibit myoblast differentiation. [score:3]
In addition, miR-203 has a significantly higher expression level in dwarf chickens than in normal chickens (Figure 1d), a finding that is consistent with our previous microarray data. [score:3]
Importantly, miR-203 in situ hybridisation in dwarf E14 leg muscle also confirmed its expression in muscle tissue (Figure 1c). [score:3]
[56] Although our results do not verify the possibility in chicken myoblasts, they provide another source of evidence to support the regulation network of miR-203, c-JUN and MEF2C during myoblast differentiation into myotubes (Figure 8). [score:2]
To observe the effects of miR-203 on myoblast proliferation, we transfected myoblasts cultured in GM with an miR-203 mimic or scrambled negative control duplexes (Figure 3a), and then monitored the proliferation status of cells using the WST-8 assay and Cell-Counting Kit-8. miR-203 was shown to significantly inhibit myoblast proliferation (Figure 3b). [score:2]
The 12- μm thick cryosections were fixed in 4% PFA for 15 min at room temperature, treated for 15 min with Proteinase K, prehybridized and hybridised at 42 °C (miR-203 and scramble), and final colour development was performed with NBT/BCIP (Roche, Basel, Switzerland). [score:2]
Therefore, we tested whether miR-203 transfection at DM4 could influence the fusion index of myoblasts at DM7. [score:1]
Primary myoblasts cultured in GM were transfected with the miR-203 mimic or control duplexes. [score:1]
Together, the data suggest that miR-203 can represses myoblast proliferation and induces cell cycle arrest. [score:1]
The number of cells in the G0/G1 stage in the miR-203 -transfected group was significantly higher than that in the control group (Figure 3e and Supplementary File 4). [score:1]
Furthermore, we also used anti-miR-203 and antagomir-NC (anti-NC) to test the impact of miR-203 loss-of-function during myoblast differentiation. [score:1]
Furthermore, the MEF2C 3'-UTR has three predicted miR-203 binding sites (Figure 7c), and site 1 is highly conserved among vertebrates (Figure 7d). [score:1]
As cell cycle arrest is a critical step in the myoblast differentiation process and miR-203 is likely to be implicated in myoblast differentiation, we studied the effects of miR-203 on myoblast differentiation. [score:1]
Furthermore, flow cytometry analysis of the cell cycle revealed that myoblasts transfected with the miR-203 mimic could arrest myoblasts in the G0/G1 stage. [score:1]
The miR-203 mimics, mimic control duplexes, antagomirs of anti-miR-203 and anti-NC were purchased from RiboBio. [score:1]
In addition, miR-203 loss-of-function by antagomir-miR-203 (anti-miR-203; Figure 3f) increased myoblast proliferation (Figure 3g) and reduced the number of cells in the G0/G1 stage (Figure 3h and Supplementary File 5). [score:1]
DF-1 cells were co -transfected with 100 ng of the wild-type or mutant 3'-UTR dual-luciferase reporter and 50 nM of the miR-203 mimic or negative control duplexes using Lipofectamine 2000 reagent in 96-well plates. [score:1]
After immunofluorescence staining, we observed that the control myoblasts formed myotubes containing many nuclei, whereas the miR-203 -transfected myoblasts remained mononucleated (Figure 4e). [score:1]
The mutant c-JUN 3'-UTR and MEF2C 3′-UTR plasmids were generated by changing the miR-203 binding site from ATTTCA to CGCGGC, and mutagenesis was performed by PCR amplification and DpnI digestion to remove the parental DNA. [score:1]
miR-203 was previously described as a skin-abundant miRNA with an important role in skin differentiation, [28] and the annotation of miR-203 in miRBase shows that it is a skin-specific miRNA. [score:1]
miR-203 represses myoblast differentiation. [score:1]
Because the 3′-UTR of MEF2C has three predicted miR-203 binding sites that are far away from each other, we generated three pmirGLO reporter vectors of the MEF2C 3′-UTR. [score:1]
Furthermore, when the predicted miR-203 seed region in the 3'-UTR was mutated, the mutant reporter no longer responded to miR-203 (Figure 5f). [score:1]
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[+] score: 118
The c-JUN and MEF2C are both direct targets of miR-203 in chickens, and their expression levels were inhibited by miR-203 (Luo et al., 2014). [score:8]
This result demonstrates that circSVIL expression is negative correlated with miR-203 levels, whose expression has been reported to downregulate from proliferation to differentiation of myoblasts (Luo et al., 2014). [score:8]
Moreover, miR-203 was also reported to express differentially during chicken embryonic skeletal muscle development and to express highly at E12 and E14 (Luo et al., 2014). [score:6]
The results that circSVIL upregulated the mRNA level of c-JUN and MEF2C also indicated that circSVIL could inhibit the activity of miR-203. [score:6]
The results that circSVIL upregulated the target genes of miR-203 also confirmed that circSVIL could sponging miR-203. [score:6]
CircSVIL increased the expression of miR-203 target genes. [score:5]
The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiation. [score:5]
In summary, we found that chicken circSVIL could inhibit the activity of miR-203 and increased the expression of its genes c-JUN and MEF2C by sponging miR-203. [score:5]
Figure 3 CircSVIL increased the expression of MEF2C and c-JUN, the target genes for miR-203. [score:5]
In zebrafish embryos, miR-203 regulates fast muscle differentiation by targeting dmrt2a (Lu et al., 2017). [score:4]
After co -transfected circSVIL with miR-203, miR-206, or miR-NC in myoblasts, immunoprecipitation of AGO2 was performed and the circSVIL expression levels were quantified by qRT–PCR and normalized to GAPDH. [score:3]
Overexpression vector of circSVIL was transfected into QM7 cells along with miR-203, miR-206, or miR-NC control. [score:3]
Through sponging miR-203, chicken circSVIL could inhibit the activity of miR-203 and thus promote skeletal muscle cell proliferation and differentiation (Figure 7). [score:3]
miR-124 and miR-203 are epigenetically silenced tumor-suppressive microRNAs in hepatocellular carcinoma. [score:3]
We predicted that it has four potential binding sites for miR-203, which has been shown to inhibit skeletal muscle proliferation and differentiation by repressing c-JUN and MEF2C (Luo et al., 2014). [score:3]
MiR-203 was well-known as a tumor suppressor, but it was found also involving in muscle development recently (Furuta et al., 2010). [score:3]
For psiCHECK-2 vector, DF-1 cells were co -transfected with reporter vector and miR-203 mimics or NC and with circSVIL overexpression vector or empty vector (EV). [score:3]
In chicken, miR-203 has been reported to inhibit the proliferation and differentiation of myoblast (Luo et al., 2014). [score:3]
MiR-203 negatively regulates the proliferation of smooth muscle cells, and was detected abundant expressed in C2C12 myoblasts, quail myoblasts and chicken skeletal muscle (Chen et al., 2006; Li et al., 2011; Liao et al., 2015). [score:3]
We used the other dual-luciferase reporter (psiCHECK-2) by inserting perfect miR-203 target sequence into the 3′ end of Renilla luciferase. [score:3]
QM7 cells were co -transfected with circSVIL overexpression vector and 3′ end biotinylated miR-203, miR-206, or miR-NC (RiboBio). [score:3]
The chicken miR-203 inhibits myoblast proliferation and differentiation (Luo et al., 2014). [score:3]
Both these two luciferase reporter assays suggested the negative effect of circSVIL expression on miR-203 activity. [score:2]
Similarly, compared to control group, the numbers of EdU-stained cells increased in overexpression group (P < 0.01) but not in co -transfected (circSVIL and miR-203) group (Figures 4C,D). [score:2]
In this study, we also found that circSVIL was involved in chicken embryonic muscle development by sponging miR-203. [score:2]
Our results suggest that circSVIL could function as miR-203 sponge and therefore promote the embryonic skeletal muscle development. [score:2]
MicroRNA-203 negatively regulates c-Abl, ERK1/2 phosphorylation, and proliferation in smooth muscle cells. [score:1]
The wild type and mutated sequences of circSVIL (harbored normal and mutated miR-203 perfected 5′ seed pairing binding site) were synthesized and cloned into the pmirGLO dual-luciferase reporter vector (Promega) using the NheI and XhoI restriction sites. [score:1]
We found circSVIL was derived from exon 6 to 14 of SVIL (Gallus_gallus-4.0/galGal4) and harbored four potential binding sites for miR-203. [score:1]
The yellow oval indicates perfected 5′ seed pairing binding site of miR-203, and blue ovals indicate other three potential binding sites of miR-203. [score:1]
Altogether, these results suggested that circSVIL promotes myoblast proliferation, and impairs the activity of miR-203 in myoblasts. [score:1]
Therefore, we hypothesize that circSVIL could functions as miR-203 sponges in chicken. [score:1]
Figure 2Chicken circSVIL interacted with miR-203. [score:1]
In addition, in myoblast were also performed to validate the relation between circSVIL and miR-203. [score:1]
After further analysis of its sequence using miRanda, circSVIL was predicted to possess a miR-203 perfected 5′ seed pairing binding sites at 1303-1309 nt (Figures 2A,B). [score:1]
For pmirGLO vector, DF-1 cells were seeded in 96-well plates and co -transfected with wild type (WT) or mutated reporter vector and miR-203 mimics or NC (negative control). [score:1]
Three other potential binding sites for miR-203 in circSVIL were also predicted using RNAhybrid (Figure 2A and Figure S2). [score:1]
CircSVIL interacts with miR-203 in myoblasts. [score:1]
The perfect match sequence of gga-miR-203 was synthesized and cloned into the psiCHECK-2 vector (Promega) using the NotI and XhoI restriction sites. [score:1]
Figure 7Mechanism of circSVIL in promoting skeletal muscle cell proliferation and differentiation through sponging miR-203. [score:1]
Therefore, circSVIL also likely to play an important role on myoblast proliferation by acts as a sponge of miR-203. [score:1]
Altogether, these results suggested that a highly efficient interaction between circSVIL and miR-203. [score:1]
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[+] score: 14
In 7-week-old chickens, as compared with 14-day-old embryos, the expression of let-7b, miR-30a-5p, miR-30b, miR-99a and miR-133b was significantly up-regulated, but miR-16c, miR-92, miR-106, miR-203, miR-451 and miR-454 were significantly down-regulated in both dwarf and normal chickens. [score:8]
The expression of miR-16c, miR-92, miR-106, miR-203, miR-451, and miR-454 was commonly down-regulated (Table  2). [score:6]
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[+] score: 13
MiR-203 is a skin- and keratinocyte-specific miRNA that has been implicated in repression of ‘stemness’ in epidermal progenitors by targeting p63 and the suppressor of cytokine signaling-3 (SOCS-3) [38]. [score:5]
Up-regulation of miR-203 is required for differentiation in human keratinocytes and is dependent on the activation of the Pkc/AP-1 pathway [39]. [score:4]
Sonkoly E Wei T Loriè EP Suzuki H Kato M Törmä H Stahle M Pivarcsi A Protein kinase C -dependent upregulation of miR-203 induces the differentiation of human keratinocytesJ Invest Dermatol. [score:4]
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[+] score: 13
Therefore, although little is known about the specific functions of several of these miRNAs (e. g. miR-31, miR-101, miR-200b, miR-10b, miR-460, miR-15b, miR-16 and miR203) during muscle development, the close relationship between their targets and myogenesis regulation demonstrates a potential role during muscle development. [score:6]
Seven (miR-101, miR-10a, miR-10b, miR-1677, let-7f, miR-31, and miR-205b) were expressed at higher levels in layers, and ten (miR-203, miR-200b, miR-16c, miR-15b, miR-15c, miR-460, miR-429, let-7c, miR-2188, and gga-miR-N2) were expressed at higher levels in broilers. [score:5]
Little is known about the functional roles of the remaining eight (miR-31, miR-101, miR-200b, miR-10b, miR-460, miR-15b, miR-16 and miR-203) during muscle development. [score:2]
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[+] score: 5
Luo W. Wu H. Ye Y. Li Z. Hao S. Kong L. Zheng X. Lin S. Nie Q. Zhang X. The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiation Cell Death Dis. [score:5]
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The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiation. [score:5]
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2010.06.013 20619301 5. Luo W The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiationCell Death Dis. [score:5]
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[+] score: 5
Luo W. Wu H. Ye Y. Li Z. Hao S. Kong L. Zheng X. Lin S. Nie Q. Zhang X. The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiation Cell Death Dis. [score:5]
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The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiation. [score:5]
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Other miRNAs from this paper: gga-mir-125b-2, gga-mir-203a, gga-mir-125b-1
Luo W. Wu H. Ye Y. Li Z. Hao S. Kong L. Zheng X. Lin S. Nie Q. Zhang X. The transient expression of miR-203 and its inhibiting effects on skeletal muscle cell proliferation and differentiationCell Death Dis. [score:5]
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[+] score: 3
Other miRNAs from this paper: gga-mir-203a
An additional control mechanism could be through the activation of miR-203 by RBM28 [36], to which the leptin receptor is a potential target [38]. [score:3]
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[+] score: 3
Additionally, miR-200a, miR-200b, miR-203, miR-27a, and miR-27b, all of which interact with Wnt signaling components [63], [64], [65], are expressed at 1.5- to 58.9-fold higher levels in duck verses the other species (Table S7). [score:3]
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Some miRNAs such as miR-203 had been previously reported as up regulated in proliferating myoblasts and down regulated during differentiation at days E14 and E16 [13]. [score:3]
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[40] It was revealed that miR-146, [41] miR-155, [42] and miR-203 [43] regulate arthritic inflammatory response. [score:2]
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We identified 23 and 19 miRNAs with significant differential abundance in the Condition and Line comparisons, respectively, with only two miRNAs (gga-let-7f and gga-miR-203) found in common between comparisons. [score:1]
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