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Cat (Feline) Monoclonal MYOD1 Primary Antibody pour ICC, IF - ABIN4337151
Sun, Ge, Drnevich, Zhao, Band, Chen: Mammalian target of rapamycin regulates miRNA-1 and follistatin in skeletal myogenesis. dans The Journal of cell biology 2010
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Chicken Monoclonal MYOD1 Primary Antibody pour IHC (fro), WB - ABIN967403
Davis, Weintraub, Lassar: Expression of a single transfected cDNA converts fibroblasts to myoblasts. dans Cell 1988
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Human Polyclonal MYOD1 Primary Antibody pour IF (cc), IF (p) - ABIN740340
Gong, Zhao, Yang, Li, Chen, Chen, Zhou: The control of mesenchymal stem cell differentiation using dynamically tunable surface microgrooves. dans Advanced healthcare materials 2014
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Human Monoclonal MYOD1 Primary Antibody pour ELISA, WB - ABIN969305
Mal: Histone methyltransferase Suv39h1 represses MyoD-stimulated myogenic differentiation. dans The EMBO journal 2006
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Human Monoclonal MYOD1 Primary Antibody pour ICC, IF - ABIN2668627
Harada, Ohkawa, Ao, Odawara, Okada, Azuma, Nishiyama, Nakamura, Tachibana: Rat monoclonal antibody specific for MyoD. dans Hybridoma (2005) 2010
Human MYOD1 Primary Antibody pour IHC - ABIN966631
Reynaud, Leibovitch, Tintignac, Pelpel, Guillier, Leibovitch: Stabilization of MyoD by direct binding to p57(Kip2). dans The Journal of biological chemistry 2000
SRF and its cofactor MYOCD (Montrer MYOCD Anticorps) 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 (Montrer CDKN1C Anticorps) 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 (Montrer FOXF1 Anticorps)-mediated Wnt5a (Montrer WNT5A Anticorps)/beta-Catenin (Montrer CTNNB1 Anticorps) signaling pathway, and suppresses GC cell apoptosis through MYOD1-mediated Caspase-3 (Montrer CASP3 Anticorps) 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 (Montrer TGFB1 Anticorps) 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 (Montrer TGFB1 Anticorps)/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 (Montrer PAX7 Anticorps)/MyoD-dependent activation of miR (Montrer MLXIP Anticorps)-182 and provide insight into the role that myogenic transcription factors have in sarcoma progression
These observations demonstrated the first time that Wnt3a (Montrer WNT3A Anticorps) can directly activate MyoD expression through targeting cis (Montrer CISH Anticorps)-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.
MyoD regulates the oxidative metabolic capacity of adult skeletal muscle;ChIP-seq analysis identified MyoD binding on the PGC (Montrer PGC Anticorps)-1b, but not PGC (Montrer PGC Anticorps)-1a, gene locus;MyoD cooperates with alternative NF-kappaB (Montrer NFKB1 Anticorps) to regulate PGC (Montrer PGC Anticorps)-1b transcription; MyoD and RelB (Montrer RELB Anticorps) co-occupy many other genes involved in aerobic respiration
LSD1 (Montrer KDM1A Anticorps) is required for the timely expression of MyoD in limb buds.
bn1 (Montrer CCR6 Anticorps) expression is induced during myoblast differentiation, in a p38 MAP kinase (Montrer MAPK14 Anticorps)- and MyoD- dependent manner. RNAi-mediated depletion of drebrin (Montrer DBN1 Anticorps), or treatment with a chemical drebrin (Montrer DBN1 Anticorps) 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 (Montrer MYOG Anticorps) associate with distinct chromatin states.
lf5 ChIP-seq revealed that Klf5 (Montrer KLF5 Anticorps) binding overlaps that of MyoD and Mef2 (Montrer MEF2C Anticorps), and Klf5 (Montrer KLF5 Anticorps) physically associates with both MyoD and Mef2 (Montrer MEF2C Anticorps). In addition, MyoD recruitment was greatly reduced in the absence of Klf5 (Montrer KLF5 Anticorps). These results indicate that Klf5 (Montrer KLF5 Anticorps) is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD and Mef2 (Montrer MEF2C Anticorps).
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 (Montrer GNAT1 Anticorps)-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 (Montrer MLXIP Anticorps)-29a-Tet1 (Montrer TET1 Anticorps) pathway upregulates MyoD expression and conversely downregulates Cdk6 (Montrer CDK6 Anticorps) expression
an Enhancer box and a binding site for a cooperative co-activator of MyoD are present in the promoter region of porcine PPARgamma (Montrer PPARG Anticorps).
Of the eight adult pig tissue types that were tested, the expression of Myf5 (Montrer MYF5 Anticorps) and MyoD1 was highest in the muscle tissue.
Single nucleotide polymorphisms in the MYOD1 and GDF8 (Montrer MSTN Anticorps) genes are associated with genetic transcription during myogenesis in pigs.
Therefore, this study demonstrated that the different regulatory adipogenic roles of MSTN (Montrer MSTN Anticorps) in ADSCs and MSCs act by differentially regulating PPARgamma (Montrer PPARG Anticorps) 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 (Montrer PAX7 Anticorps) 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 (Montrer UTS2R Anticorps) region of this gene.
Relative MYOD1 expression was not different, but MYOG (Montrer MYOG Anticorps) 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 (Montrer MYF5 Anticorps) activates MYF5 (Montrer MYF5 Anticorps) and MYOD1 expression in cultured fibroblasts.
results suggest that MyoD and Myf5 (Montrer MYF5 Anticorps) influence the MyHC (Montrer MYH13 Anticorps) 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 (Montrer MKX Anticorps) 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 (Montrer CDKN1C Anticorps), thereby providing a positive feedback loop that switches myogenic cells to terminal differentiation
Myf5 (Montrer MYF5 Anticorps) 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