ArticleMolecular and cellular biology2004
Mutant MyoD lacking Cdc2 phosphorylation sites delays M-phase entry.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Emerin loss of function inhibits MyoD-driven differentiation of human iPSCs into skeletal myotubes.bioRxiv : the preprint server for biology · 2026Article
- Migration and differentiation of muscle stem cells are coupled by RhoA signalling during regeneration.Open biology · 2023Article
- DNA-PKcs regulates myogenesis in an Akt-dependent manner independent of induced DNA damage.Cell death and differentiation · 2023Article
- Palmitic Acid Inhibits Myogenic Activity and Expression of Myosin Heavy Chain MHC IIb in Muscle Cells through Phosphorylation-Dependent MyoD Inactivation.International journal of molecular sciences · 2023Article
- Intravital imaging reveals cell cycle-dependent myogenic cell migration during muscle regeneration.Cell cycle (Georgetown, Tex.) · 2020Article
- CK2-Dependent Phosphorylation of the Brg1 Chromatin Remodeling Enzyme Occurs during Mitosis.International journal of molecular sciences · 2020Article
- iPTMnet: an integrated resource for protein post-translational modification network discovery.Nucleic acids research · 2018Article
- MyoD phosphorylation on multiple C terminal sites regulates myogenic conversion activity.Biochemical and biophysical research communications · 2016Article
- Phosphorylation-dependent degradation of MEF2C contributes to regulate G2/M transition.Cell cycle (Georgetown, Tex.) · 2015Article
- Direct reprogramming of fibroblasts to myocytes via bacterial injection of MyoD protein.Cellular reprogramming · 2013Article
- Human NDR kinases control G(1)/S cell cycle transition by directly regulating p21 stability.Molecular and cellular biology · 2011Article
- Conditional TGF-β1 treatment increases stem cell-like cell population in myoblasts.Journal of cellular and molecular medicine · 2011Article
- Secretome Analysis of Skeletal Myogenesis Using SILAC and Shotgun Proteomics.International journal of proteomics · 2011Article
- Mammalian target of rapamycin regulates miRNA-1 and follistatin in skeletal myogenesis.The Journal of cell biology · 2010Article
- Down-regulation of MyoD by calpain 3 promotes generation of reserve cells in C2C12 myoblasts.The Journal of biological chemistry · 2010Article
- p38-{gamma}-dependent gene silencing restricts entry into the myogenic differentiation program.The Journal of cell biology · 2009Article
- Article
- Inhibition of atrogin-1/MAFbx mediated MyoD proteolysis prevents skeletal muscle atrophy in vivo.PloS one · 2009Article
- Multiple phosphorylation events control mitotic degradation of the muscle transcription factor Myf5.BMC biochemistry · 2005Article
- Conditional transgenic system for mouse aurora a kinase: degradation by the ubiquitin proteasome pathway controls the level of the transgenic protein.Molecular and cellular biology · 2005Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factors MyoD and Myf-5 control myoblast identity and differentiation. MyoD and Myf-5 manifest opposite cell cycle-specific expression patterns. Here, we provide evidence that MyoD plays a pivotal role at the G(2)/M transition by controlling the expression of p21(Waf1/Cip1) (p21), which is believed to regulate cyclin B-Cdc2 kinase activity in G(2). In growing myoblasts, MyoD reaccumulates during G(2) concomitantly with p21 before entry into mitosis; MyoD is phosphorylated on Ser5 and Ser200 by cyclin B-Cdc2, resulting in a decrease of its stability and down-regulation of both MyoD and p21. Inducible expression of a nonphosphorylable MyoD A5/A200 enhances the MyoD interaction with the coactivator P/CAF, thereby stimulating the transcriptional activation of a luciferase reporter gene placed under the control of the p21 promoter. MyoD A5/A200 causes sustained p21 expression, which inhibits cyclin B-Cdc2 kinase activity in G(2) and delays M-phase entry. This G(2) arrest is not observed in p21(-/-) cells. These results show that in cycling cells MyoD functions as a transcriptional activator of p21 and that MyoD phosphorylation is required for G(2)/M transition.
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