p53 protein is a key regulatory component of a stress-inducible cell-cycle checkpoint pathway in mammalian cells, which can promote either cell-growth arrest or apoptosis, depending on the type of cell and damaging agent utilized. Environmental insults that can activate the p53 pathway are quite distinct, and include ionizing and nonionizing radiation (1 –5 ), antimetabolites which inhibit ribonucleotide biosynthesis (6 ), inhibitors of spindle formation (7 ), microtubule-affecting drugs (8 ), factors inducing differentiation (9 ), signaling pathways activated in transformed cells during anchorage-independent growth (10 ), heat shock (11 ), and hypoxia (12 ).
