The nuclear p300/CBP proteins function as coactivators of gene transcriptio
n. Here, using cells deficient in p300 or CBP, we show that p300, and not C
BP, is essential for ionizing radiation-induced accumulation of the p53 tum
or suppressor and thereby p53-mediated growth arrest. The results demonstra
te that deficiency of p300 results in increased degradation of p53. Our fin
dings suggest that p300 contributes to the stabilization and transactivatio
n function of p53 in the cellular response to DNA damage.