ArticleThe Journal of cell biology2000
p21 and retinoblastoma protein control the absence of DNA replication in terminally differentiated muscle cells.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Cyclin D3 Colocalizes with Myogenin and p21 in Skeletal Muscle Satellite Cells during Early-Stage Functional Overload.Acta histochemica et cytochemica · 2023Article
- Identification of MyoD-Responsive Transcripts Reveals a Novel Long Non-coding RNA (lncRNA-AK143003) that Negatively Regulates Myoblast Differentiation.Scientific reports · 2017Article
- G9a promotes proliferation and inhibits cell cycle exit during myogenic differentiation.Nucleic acids research · 2016Article
- Using the E4orf6-Based E3 Ubiquitin Ligase as a Tool To Analyze the Evolution of Adenoviruses.Journal of virology · 2016Article
- p38α MAPK disables KMT1A-mediated repression of myogenic differentiation program.Skeletal muscle · 2016Article
- Nutlin-3 down-regulates retinoblastoma protein expression and inhibits muscle cell differentiation.Biochemical and biophysical research communications · 2015Article
- Aberrant cell cycle reentry in human and experimental inclusion body myositis and polymyositis.Human molecular genetics · 2014Article
- The p44/wdr77-dependent cellular proliferation process during lung development is reactivated in lung cancer.Oncogene · 2013Article
- Modulation of cell cycle progression by 5-azacytidine is associated with early myogenesis induction in murine myoblasts.International journal of biological sciences · 2013Article
- Degradation of p21Cip1 through anaphase-promoting complex/cyclosome and its activator Cdc20 (APC/CCdc20) ubiquitin ligase complex-mediated ubiquitylation is inhibited by cyclin-dependent kinase 2 in cardiomyocytes.The Journal of biological chemistry · 2011Article
- The dynamics of E1A in regulating networks and canonical pathways in quiescent cells.BMC research notes · 2011Article
- E1A interacts with two opposing transcriptional pathways to induce quiescent cells into S phase.Journal of virology · 2010Article
- Activation of Cdc6 by MyoD is associated with the expansion of quiescent myogenic satellite cells.The Journal of cell biology · 2010Article
- MLL5, a trithorax homolog, indirectly regulates H3K4 methylation, represses cyclin A2 expression, and promotes myogenic differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Adenovirus E1B55K region is required to enhance cyclin E expression for efficient viral DNA replication.Journal of virology · 2008Article
- pRb-dependent cyclin D3 protein stabilization is required for myogenic differentiation.Molecular and cellular biology · 2007Article
- Critical requirement for cell cycle inhibitors in sustaining nonproliferative states.The Journal of cell biology · 2007Article
- Review
- Histone methyltransferase Suv39h1 represses MyoD-stimulated myogenic differentiation.The EMBO journal · 2006Article
- Mirk/Dyrk1B mediates survival during the differentiation of C2C12 myoblasts.The Journal of biological chemistry · 2005Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
During differentiation, skeletal muscle cells withdraw from the cell cycle and fuse into multinucleated myotubes. Unlike quiescent cells, however, these cells cannot be induced to reenter S phase by means of growth factor stimulation. The studies reported here document that both the retinoblastoma protein (Rb) and the cyclin-dependent kinase (cdk) inhibitor p21 contribute to this unresponsiveness. We show that the inactivation of Rb and p21 through the binding of the adenovirus E1A protein leads to the induction of DNA replication in differentiated muscle cells. Moreover, inactivation of p21 by E1A results in the restoration of cyclin E-cdk2 activity, a kinase made nonfunctional by the binding of p21 and whose protein levels in differentiated muscle cells is relatively low in amount. We also show that restoration of kinase activity leads to the phosphorylation of Rb but that this in itself is not sufficient for allowing differentiated muscle cells to reenter the cell cycle. All the results obtained are consistent with the fact that Rb is functioning downstream of p21 and that the activities of these two proteins may be linked in sustaining the postmitotic state.
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Registered trials
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