p53-independent expression of p21Cip1 in muscle and other terminally differentiating cells

Susan B. Parker, Gregor Eichele, Pumin Zhang, Alan Rawls, Arthur T. Sands, Allan Bradley, Eric N. Olson, J. Wade Harper, Stephen J. Elledge

Research output: Contribution to journalArticlepeer-review

1027 Scopus citations


Terminal differentiation is coupled to withdrawal from the cell cycle. The cyclin-dependent kinase inhibitor (CKI) p21Cip1 is transcriptionally regulated by p53 and can induce growth arrest. CKIs are therefore potential mediators of developmental control of cell proliferation. The expression pattern of mouse p21 correlated with terminal differentiation of multiple cell lineages including skeletal muscle, cartilage, skin, and nasal epithelium in a p53-independent manner. Although the muscle-specific transcription factor MyoD is sufficient to activate p21 expression in 10T1/2 cells, p21 was expressed in myogenic cells of mice lacking the genes encoding MyoD and myogenin, demonstrating that p21 expression does not require these transcription factors. The p21 protein may function during development as an inducible growth inhibitor that contributes to cell cycle exit and differentiation.

Original languageEnglish (US)
Pages (from-to)1024-1027
Number of pages4
Issue number5200
StatePublished - 1995
Externally publishedYes

ASJC Scopus subject areas

  • General


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