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pubmed-article:8118801pubmed:abstractTextThe tumor growth suppressor WAF1/CIP1 was recently shown to be induced by p53 and to be a potent inhibitor of cyclin-dependent kinases. In the present studies, we sought to determine the relationship between the expression of WAF1/CIP1 and endogenous regulation of p53 function. WAF1/CIP1 protein was first localized to the nucleus of cells containing wild-type p53 and undergoing G1 arrest. WAF1/CIP1 was induced in wild-type p53-containing cells by exposure to DNA damaging agents, but not in mutant p53-containing cells. The induction of WAF1/CIP1 protein occurred in cells undergoing either p53-associated G1 arrest or apoptosis but not in cells induced to arrest in G1 or to undergo apoptosis through p53-independent mechanisms. DNA damage led to increased levels of WAF1/CIP1 in cyclin E-containing complexes and to an associated decrease in cyclin-dependent kinase activity. These results support the idea that WAF1/CIP1 is a critical downstream effector in the p53-specific pathway of growth control in mammalian cells.lld:pubmed
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pubmed-article:8118801pubmed:articleTitleWAF1/CIP1 is induced in p53-mediated G1 arrest and apoptosis.lld:pubmed
pubmed-article:8118801pubmed:affiliationOncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231.lld:pubmed
pubmed-article:8118801pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8118801pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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