Radiation-induced cell cycle arrest compromised by p21 deficiency
摘要:
THE protein p21 is a dual inhibitor of cyclin-dependent kinases 1á¤-3 and proliferating-cell nuclear antigen (PCNA) 4 , both of which are required for passage through the cell cycle. The p21 gene is under the transcriptional control of p53 (ref. 5), suggesting that p21 might promote p53-dependent cell cycle arrest or apoptosis. p21 has also been implicated in cell senescence 6 and in cell-cycle withdrawal upon terminal differentiation 7á¤-9 . Here we investigate the role of p21 in these processes using chimaeric mice composed partly of p21 -/- and partly of p21 +/+ cells. Immunohistochemical studies of the p21 +/+ and p21 -/- components of adult small intestine indicated that deletion of p21 had no detectable effect on the migration-associated differentiation of the four principal intestinal epithelial cell lineages or on p53-dependent apoptosis following irradiation. However, p21 -/- mouse embryo fibroblasts are impaired in their ability to undergo Gl arrest following DNA damage.
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DOI:
10.1038/377552a0
被引量:
年份:
1995










































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