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The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Correlation of Terminal Cell Cycle Arrest of Skeletal Muscle with Induction of p21 by MyoD

Halevy, Orna, Novitch, Bennett G., Spicer, Douglas B., Skapek, Stephen X., Rhee, James, Hannon, Gregory J., Beach, David, Lassar, Andrew B.·1995·Science

Abstract

Skeletal muscle differentiation entails the coordination of muscle-specific gene expression and terminal withdrawal from the cell cycle. This cell cycle arrest in the G0 phase requires the retinoblastoma tumor suppressor protein (Rb). The function of Rb is negatively regulated by cyclin-dependent kinases (Cdks), which are controlled by Cdk inhibitors. Expression of MyoD, a skeletal muscle-specific transcriptional regulator, activated the expression of the Cdk inhibitor p21 during differentiation of murine myocytes and in nonmyogenic cells. MyoD-mediated induction of p21 did not require the tumor suppressor protein p53 and correlated with cell cycle withdrawal. Thus, MyoD may induce terminal cell cycle arrest during skeletal muscle differentiation by increasing the expression of p21.

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Metadata

Authors
Halevy, O., Novitch, B. G., Spicer, D. B., Skapek, S. X., Rhee, J., Hannon, G. J., Beach, D., & Lassar, A. B.
Venue
Science
Published
1995-02-17
Volume
267
Issue
5200
Pages
1018-1021
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2052651806
Cited by
1,149
References
5
FWCI
43.10
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Correlation of Terminal Cell Cycle Arrest of Skeletal Muscle with Induction of p21 by MyoD. https://app.cochat.ai/papers/10.1126/science.7863327
The paper
Halevy, O., Novitch, B. G., Spicer, D. B., Skapek, S. X., Rhee, J., Hannon, G. J., Beach, D., & Lassar, A. B. (1995). Correlation of Terminal Cell Cycle Arrest of Skeletal Muscle with Induction of p21 by MyoD. Science. https://doi.org/10.1126/science.7863327

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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