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SRF and its cofactor MYOCD likely contribute to the hypertrophy of peripheral airway smooth muscle observed in equine asthmatic airways, while the remodeling of the central airways is more static or involves different transcription factors.
Equine primary fibroblasts were transformed by lentiviral transduction of equine myogenic differentiation 1 into fusion-competent myoblasts.
The results strongly suggest that the combination of MYCL plus MYOD1 may promote direct conversion of human fibroblasts into functional myoblasts that could potentially be used for regenerative therapy for muscle diseases and congenital muscle defects.
Analysis of the chromatin status of Cdkn1c (show CDKN1C Proteins) promoter and KvDMR1 in unresponsive compared to responsive cell types showed that their differential responsiveness to the MyoD-dependent induction of the gene does not involve just their methylation status but, rather, the differential H3 lysine 9 dimethylation at KvDMR1.
Data show that MeCP2 promotes gastric cancer (GC) cell proliferation via FOXF1 (show FOXF1 Proteins)-mediated Wnt5a (show WNT5A Proteins)/beta-Catenin (show CTNNB1 Proteins) signaling pathway, and suppresses GC cell apoptosis through MYOD1-mediated Caspase-3 (show CASP3 Proteins) signaling pathway.
Our results on Pax7 and MyoD protein expression suggest that proliferation and differentiation of skeletal muscle stem cells are affected in ALS patients, and the myogenic processes cannot overcome the denervation-induced wasting.
The molecular pathogenesis of radiotherapy-induced muscle fibrosis involves the TGF-beta1 (show TGFB1 Proteins) pathway and its repression of MyoD expression. Our results suggest a correlation between traditional swallow therapy /neuromuscular electrical stimulation combined therapy and the restoration of TGF-beta1 (show TGFB1 Proteins)/MyoD homeostasis in cervical muscles.
Unmethylated MYOD1 gene is associated with chemoradiation resistance in Invasive Cervical Carcinoma.
We provide the first description of a human phenotype that appears to result from MYOD1 mutation. The presentation with Lethal fetal akinesia deformation sequence is consistent with a large body of data demonstrating that in the mouse, MyoD is a major controller of precursor cell commitment to the myogenic differentiation programme
these results suggest that sarcoma metastasis can be partially controlled through Pax7 (show PAX7 Proteins)/MyoD-dependent activation of miR (show MLXIP Proteins)-182 and provide insight into the role that myogenic transcription factors have in sarcoma progression
These observations demonstrated the first time that Wnt3a (show WNT3A Proteins) can directly activate MyoD expression through targeting cis (show CISH Proteins)-elements in the DE and the L fragment.
Studies indicate that MyoD occupies multiple promoters that induce the transcription of genes vital for establishing the myogenic fate and is also implicated as a mediator of many chromatin modifying enzymes for their recruitment to myogenic enhancers.
Results indicate the importance of integrating histone modifications and MyoD chromatin binding for coordinated gene activation and repression during myogenic differentiation.
Data suggest Tle3 plays role in regulation of MyoD1 function during myogenesis; up-regulation of Tle3 expression suppresses myogenesis; conversely, down-regulation of Tle3 expression promotes myogenesis/cell proliferation; Tle3 interferes with MyoD1 by disrupting association of basic helix-loop-helix domain of MyoD with E proteins. (Tle3 = transducin (show GNAT1 Proteins)-like enhancer of split 3; MyoD1 = myogenic differentiation protein 1)
significant co-localization of binding sites for MyoD and Six proteins on over a thousand mouse genomic DNA regions, were found.
Through mutational analysis, we derive an optimally active phospho-mutant form of MyoD that has a dramatically enhanced ability to drive myogenic reprogramming in vivo. Mechanistically, this is achieved through increased protein stability and enhanced chromatin association. Therefore, multi-site phospho-regulation of class II bHLH proteins is conserved across cell lineages and germ layers, and manipulation of phosphorylat
results suggest that the miR (show MLXIP Proteins)-29a-Tet1 (show TET1 Proteins) pathway upregulates MyoD expression and conversely downregulates Cdk6 (show CDK6 Proteins) expression
Data show that myoblast determination protein 1 (MyoD) acts partially through microRNA miR (show MLXIP Proteins)-133 to suppress brown adipocyte cell fate.
This evidence demonstrates that TBP2 (show Tbpl2 Proteins) does not replace TBP (show TBP Proteins) during muscle differentiation, as previously proposed, with limiting amounts of TFIID-TBP (show TBP Proteins) being required to promote muscle-specific (show EIF3K Proteins) gene expression
established a model in which FHL3 (show FHL3 Proteins) promotes the expression of MyHC 2a (show MYH2 Proteins) through CREB (show CREB1 Proteins)-mediated transcription and inhibits the expression of MyHC 1/slow by inhibiting MyoD transcription activity during myogenesis
Transcription of the skeletal muscle program is achieved by the expression of MyoD, which binds to the same sites as Myf5 (show MYF5 Proteins), indicating that each factor regulates distinct steps in gene initiation and transcription at a shared set of binding sites
The large TBP polyQ repeat decreases the association of MyoD with TBP and DNA promoters and causes muscle degeneration in spinocerebellar ataxia 17 transgenic mice.
an Enhancer box and a binding site for a cooperative co-activator of MyoD are present in the promoter region of porcine PPARgamma (show PPARG Proteins).
Of the eight adult pig tissue types that were tested, the expression of Myf5 (show MYF5 Proteins) and MyoD1 was highest in the muscle tissue.
Single nucleotide polymorphisms in the MYOD1 and GDF8 (show MSTN Proteins) genes are associated with genetic transcription during myogenesis in pigs.
Therefore, this study demonstrated that the different regulatory adipogenic roles of MSTN (show MSTN Proteins) in ADSCs and MSCs act by differentially regulating PPARgamma (show PPARG Proteins) and MyoD expression.
Therefore, the g.489C>T and g.1264C>A SNPs in MYOD1 may be meaningful DNA markers that can be used for improving important porcine economic traits.
The total expression profile of MyoD and Pax7 (show PAX7 Proteins) genes suggests that higher muscularity in Pietrain pigs is associated with the presence of a greater number of active satellite stem cells compared to other breeds.
Exons and promoters are amplified and sequenced in the 5'UTR region of this gene.
Relative MYOD1 expression was not different, but MYOG (show MYOG Proteins) expression was higher in the (ligated-tube)crowded group embryos.
MYOD1 intron 1 DdeI polymorphism was not significantly associated with any meat quality traits tested
Transcript abundance for the muscle regulatory gene MYOD1 was lower in animals with more tender beef.
Bos taurus MYF5 (show MYF5 Proteins) activates MYF5 (show MYF5 Proteins) and MYOD1 expression in cultured fibroblasts.
results suggest that MyoD and Myf5 influence the MyHC isoform expression, although the effects are not decisive in specifying the phenotypes of adult muscles
n conclusion, hypoxia stimulates the proliferation of satellite cells and promotes their myogenic differentiation with MyoD playing an important role
Irxl1/Mkx (show MKX Proteins) can repress myoD expression through direct binding to its promoter and may thus play a negative regulatory role in muscle differentiation.
Myod in turn up-regulates cdkn1c (show CDKN1C Proteins), thereby providing a positive feedback loop that switches myogenic cells to terminal differentiation
Myf5 (show MYF5 Proteins) and Myod function independently during cranial myogenesis.
This gene encodes a nuclear protein that belongs to the basic helix-loop-helix family of transcription factors and the myogenic factors subfamily. It regulates muscle cell differentiation by inducing cell cycle arrest, a prerequisite for myogenic initiation. The protein is also involved in muscle regeneration. It activates its own transcription which may stabilize commitment to myogenesis.
myogenic factor 3
, myogenic differentiation 1
, myoblast determination protein 1
, MYOD protein
, myogenic factor MyoD1
, MYOD1 homolog
, myoblast determination protein 1 homolog
, myogenic factor 1
, class C basic helix-loop-helix protein 1
, myogenic regulatory factor
, myogenic differenciation 1, transcription activator
, myogenic differenciation 1
, myoblast determination 1