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Myogenic differentiation 1

MyoD, MyoD1
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Myogenin, CAN, Myf5, PAX7, HAD
Papers using MyoD antibodies
A dual epigenomic approach for the search of obesity biomarkers: DNA methylation in relation to diet-induced weight loss
Dhar M. S. et al., In Journal of Nutrition and Metabolism, 2010
... MyoD and Atp10c were from Qiagen (Valencia, CA) ...
Genetic ablation of complement C3 attenuates muscle pathology in dysferlin-deficient mice.
Agarwal Sudha, In PLoS ONE, 2009
... , and MyoD-hBcl-2 transgenic mice that overexpress human ...
Dysregulation of cardiogenesis, cardiac conduction, and cell cycle in mice lacking miRNA-1-2
Chen Jie et al., In The Journal of Cell Biology, 2006
... The antibodies were obtained from the following sources: anti-tubulin was obtained from Abcam, anti-MyoD (5.8A) was obtained from Imgenex, antibodies against HDAC4, mTOR, ...
Salamander limb regeneration involves the activation of a multipotent skeletal muscle satellite cell population
Simon András et al., In The Journal of Cell Biology, 2003
... Invitrogen), rabbit polyclonal anti-H3P antibody (Upstate Biotechnology), rat monoclonal anti-BrdU IgG (Trichem ApS), rabbit polyclonal anti-MyoD antibody (Santa Cruz Biotechnology, Inc.), anti-WE3 monoclonal IgG ...
The cxc chemokine cCAF stimulates differentiation of fibroblasts into myofibroblasts and accelerates wound closure
Martins-Green Manuela et al., In The Journal of Cell Biology, 1998
... used were: anti–α-SMA (Sigma-Aldrich); anti-TGFβ 1,2,3 (R&D Systems); antivimentin, antidesmin, antimyosin heavy chain (Hybridoma Bank); anti-myoD (Santa Cruz Biotechnology, Inc.); anti–mouse horseradish peroxidase, ...
Papers on MyoD
Contrasting roles for MyoD in organizing myogenic promoter structures during embryonic skeletal muscle development.
Imbalzano et al., Worcester, United States. In Dev Dyn, 20 Nov 2014
The lineage-determining factor MyoD is bound to myogenic genes at the onset of differentiation whether gene activation is immediate or delayed.
CCN family protein 2 (CCN2) promotes the early differentiation, but inhibits the terminal differentiation of skeletal myoblasts.
Takigawa et al., Okayama, Japan. In J Biochem, 26 Oct 2014
Recombinant CCN2 (rCCN2) promoted proliferation and MyoD production in C2C12 cells and primary myoblasts, but inhibited myogenin production.
The Hippo transducer YAP1 transforms activated satellite cells and is a potent effector of embryonal rhabdomyosarcoma formation.
Camargo et al., Boston, United States. In Cancer Cell, 11 Sep 2014
YAP1-TEAD1 upregulate pro-proliferative and oncogenic genes and maintain the ERMS differentiation block by interfering with MYOD1 and MEF2 pro-differentiation activities.
Molecular cloning and expression pattern of duck Six1 and its preliminary functional analysis in myoblasts transfected with eukaryotic expression vector.
Wang et al., In Indian J Biochem Biophys, Aug 2014
The expression profiles of Six1, Myf5 and MyoD showed that their expression levels were significantly increased.
A recurrent neomorphic mutation in MYOD1 defines a clinically aggressive subset of embryonal rhabdomyosarcoma associated with PI3K-AKT pathway mutations.
Ladanyi et al., New York City, United States. In Nat Genet, Jun 2014
Whereas ARMS tumors typically contain translocations generating PAX3-FOXO1 or PAX7-FOXO1 fusions that block terminal myogenic differentiation, no functionally comparable genetic event has been found in ERMS tumors.
Role of skeletal muscle in mandible development.
Kablar et al., Halifax, Canada. In Histol Histopathol, Jun 2014
Previous analysis of Myf5-/-:MyoD-/- mouse fetuses lacking skeletal muscle demonstrated the importance of muscle contraction and static loading in mouse skeletogenesis.
Gene regulatory networks and transcriptional mechanisms that control myogenesis.
Rigby et al., Paris, France. In Dev Cell, Mar 2014
Myogenic determination and subsequent differentiation depend on members of the MyoD family.
Metanephric adenosarcoma: a rare case with immunohistochemistry and molecular analysis.
Zhu et al., Wuhan, China. In Diagn Pathol, Dec 2013
The epithelial component was positive for CD57, AE1/AE3, but negative for WT-1, CD56, SYN, and CgA; whereas the sarcomatous component was negative for epithelial markers, SMA, Caldesmon, MyoD1, Myogenin, and S-100; and positive for vimentin, CD10, and WT1 focally.
Motoneuronal and muscle-selective removal of ALS-related misfolded proteins.
Poletti et al., Milano, Italy. In Biochem Soc Trans, Dec 2013
MyoD, myogenin, atrogin-1, TGFβ1 (transforming growth factor β1) and components of the cell response to proteotoxicity [HSPB8 (heat shock 22kDa protein 8), Bag3 (Bcl-2-associated athanogene 3) and p62] are all up-regulated by mutSOD1 in skeletal muscle.
The SWI/SNF Subunit/Tumor Suppressor BAF47/INI1 Is Essential in Cell Cycle Arrest upon Skeletal Muscle Terminal Differentiation.
Ait-Si-Ali et al., Paris, France. In Plos One, Dec 2013
Here, we show that the master myogenic differentiation factor MyoD interacts with more than one SWI/SNF subunit, including the catalytic subunit BRG1, BAF53a and the tumor suppressor BAF47/INI1.
[Regulation of differentiation of mesenchymal stem cells by the Hippo pathway effectors TAZ/YAP].
Teng et al., Harbin, China. In Yi Chuan, Nov 2013
It has been reported that the lineage-specific transcriptional factors including Runt related transcription factor 2 (RUNX2), Peroxisome proliferator-activator receptor gamma (PPARgamma) and Myogenic differentiation 1 (MyoD) may play key regulatory roles among the differentiation of MSCs.
Spindle cell rhabdomyosarcoma: a brief diagnostic review and differential diagnosis.
Nodit et al., Knoxville, United States. In Arch Pathol Lab Med, Aug 2013
Immunohistochemical workup demonstrates sarcomeric differentiation with reactivity for desmin, myogenin, and MyoD1 markers.
Coordination of satellite cell activation and self-renewal by Par-complex-dependent asymmetric activation of p38α/β MAPK.
Olwin et al., Boulder, United States. In Cell Stem Cell, 2012
Asymmetric localization of the Par complex activates p38α/β MAPK in only one daughter cell, inducing MyoD, which permits cell cycle entry and generates a proliferating myoblast.
Interplay between two myogenesis-related proteins: TBP-interacting protein 120B and MyoD.
Tamura et al., Chiba, Japan. In Gene, 2012
results suggest that MyoD and TIP120B potentiate each other at gene expression and post-translation levels, respectively, which may promote myogenesis cooperatively
Snail regulates MyoD binding-site occupancy to direct enhancer switching and differentiation-specific transcription in myogenesis.
Rudnicki et al., Ottawa, Canada. In Mol Cell, 2012
In primary myoblasts, snail-HDAC1/2 repressive complex binds and excludes MyoD from its targets.
Myo/Nog cells in normal, wounded and tumor-bearing skin.
George-Weinstein et al., In Exp Dermatol, 2012
Myo/Nog cells are the primary source of noggin in telogen hair follicles.
Muscle function and running activity in mouse models of hereditary muscle dystrophy: impact of double knockout for dystrophin and the transcription factor MyoD.
Gielen et al., Leipzig, Germany. In Muscle Nerve, 2012
mdx:myoD(-/-) is not a suitable model to study exercise-induced effects on dystrophic muscles
Finding MyoD with a little help from my friends.
Lassar, Boston, United States. In Nat Cell Biol, 2012
Findings indicate that MyoD activates the expression of other muscle regulators such as MEF2 and myogenin, which are necessary for induction of the skeletal muscle differentiation program.
Polycomb-repressed genes have permissive enhancers that initiate reprogramming.
Jones et al., Los Angeles, United States. In Cell, 2012
Using MYOD1, study shows that an nucleosome-depleted region at the minimal enhancer region allows reprogramming to be initiated, which occurs in response to signals such as the forced expression of Myod1 in fibroblasts.
Cell fate plug and play: direct reprogramming and induced pluripotency.
Studer et al., New York City, United States. In Cell, 2011
Building on the discovery that MyoD expression reprograms fibroblasts into muscle, three papers (Vierbuchen et al., 2010; Ieda et al., 2010; Szabo et al., 2010) recently reported the reprogramming of fibroblasts into neurons, cardiomyocytes, and blood cell progenitors without first passing the cells through a pluripotent state.
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