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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.
We address this paradox using basic helix-loop-helix (bHLH) transcription factors ASCL1, ASCL2, and MYOD1, crucial mediators of lineage specification..Although the ASCL factors and MYOD1 have some distinct DNA motif preference, it is not sufficient to explain the extent of the differential binding. All three factors can bind inaccessible chromatin and induce changes in chromatin accessibility and H3K27ac
ACL regulates the net amount of acetyl groups available, leading to alterations in acetylation of H3(K9/14) and H3(K27) at the MYOD locus, thus increasing MYOD expression.
we found that MYOD transcription factor can upregulate miR-223 expression by binding to an E-box region of the gga-miR-223 gene promoter during avian myoblast differentiation. IGF2 and ZEB1 are two target genes of miR-223
A high extent more than 25% of BRAF(V600E) alleles may be associated with disease outcome in PTC patients.
we present the first report of MYOD1 (L122R) mutation in the largest cohort of 49 rhabdomyosarcomas reported so far, that are associated with a relatively aggressive clinical course
Analysis of human rhabdomyosarcoma revealed that MYF5 and MYOD are mutually-exclusively expressed and each is required for sustained tumor growth.
Cell transdifferentiation of primary skin fibroblasts by forced expression of myogenic transcription factor MyoD was performed by quantitative analyses of gene expression and chromatin accessibility profiles.
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 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-mediated Wnt5a/beta-Catenin signaling pathway, and suppresses GC cell apoptosis through MYOD1-mediated Caspase-3 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 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/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/MyoD-dependent activation of miR-182 and provide insight into the role that myogenic transcription factors have in sarcoma progression
The mechanism of bakuchiol-induced myogenesis is described.
These observations demonstrated the first time that Wnt3a can directly activate MyoD expression through targeting cis-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.
MUNC is not a classic cis-acting enhancer RNA (e-RNA) acting exclusively by stimulating the neighboring MyoD gene
MyoD acts to promote SC proliferation and transition of cells into differentiation, while myogenin is known to drive terminal differentiation
Linc-RAM regulates expression of myogenic genes by directly binding MyoD, which in turn promotes the assembly of the MyoD-Baf60c-Brg1 complex on the regulatory elements of target genes.
Studies indicate MyoD displays function to regulate determination of skeletal muscle progenitors [Review].
Muscle regulatory transcription factor MyoD regulates the expression of the pro-apoptotic Bcl2 family member PUMA by binding to the promoter region of PUMA. The increase in MyoD binding to the PUMA promoter as a consequence of culture in differentiation media (DM) is diminished in myoblasts silenced for MyoD expression. In myoblasts silenced for MyoD expression, p53 binding to the PUMA promoter is diminished in response
our results indicate that HDAC11 would suppress myoblast differentiation via regulation of MyoD-dependent transcription. These findings suggest that HDAC11 is a novel critical target for controlling myoblast differentiation.
The data showed that Mettl3 is required for MyoD mRNA expression in proliferative myoblasts.
Gm7325, as a novel MyoD-target gene, is specifically induced in activated satellite cells, and may have an important role in skeletal myogenesis.
The ELF-EMFs did not affect C2C12 myoblast viability or proliferation rate. Conversely, at ELF-EMF intensity in the mT range, the myogenic process was accelerated, through increased expression of MyoD, myogenin, and connexin 43
In this study, we identified ubiquitin-specific protease 4 (USP4), one of deubiquitinating enzymes, as a suppressor of MRFs by demonstrating that a knockdown of USP4 enhances myogenesis by controlling MyoD and the level of myogenesis marker proteins in C2C12 cells... we propose that USP4 is a key player in myogenic differentiation; it controls myogenic regulatory factors in a catalytic-independent manner
MyoD regulates the oxidative metabolic capacity of adult skeletal muscle;ChIP-seq analysis identified MyoD binding on the PGC-1b, but not PGC-1a, gene locus;MyoD cooperates with alternative NF-kappaB to regulate PGC-1b transcription; MyoD and RelB co-occupy many other genes involved in aerobic respiration
LSD1 is required for the timely expression of MyoD in limb buds.
bn1 expression is induced during myoblast differentiation, in a p38 MAP kinase- and MyoD- dependent manner. RNAi-mediated depletion of drebrin, or treatment with a chemical drebrin inhibitor, resulted in a similar phenotype in myoblasts: defective differentiation, with low levels of early and late differentiation markers and inefficient production of myofibers.
Data show that MyoD and myogenin associate with distinct chromatin states.
lf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD and Mef2, and Klf5 physically associates with both MyoD and Mef2. In addition, MyoD recruitment was greatly reduced in the absence of Klf5. These results indicate that Klf5 is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD and Mef2.
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-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-29a-Tet1 pathway upregulates MyoD expression and conversely downregulates Cdk6 expression
Data show that myoblast determination protein 1 (MyoD) acts partially through microRNA miR-133 to suppress brown adipocyte cell fate.
an Enhancer box and a binding site for a cooperative co-activator of MyoD are present in the promoter region of porcine PPARgamma.
Of the eight adult pig tissue types that were tested, the expression of Myf5 and MyoD1 was highest in the muscle tissue.
Single nucleotide polymorphisms in the MYOD1 and GDF8 genes are associated with genetic transcription during myogenesis in pigs.
Therefore, this study demonstrated that the different regulatory adipogenic roles of MSTN in ADSCs and MSCs act by differentially regulating PPARgamma 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 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.
SKIP might play a role in the regulation of skeletal muscle development in pigs.
Exons and promoters are amplified and sequenced in the 5'UTR region of this gene.
Relative MYOD1 expression was not different, but MYOG 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 activates MYF5 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 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, thereby providing a positive feedback loop that switches myogenic cells to terminal differentiation
Myf5 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