Role for p300 in stabilization of p53 in the response to DNA damage.
The nuclear p300/CBP proteins function as coactivators of gene transcription. Here, using cells deficient in p300 or CBP, we show that p300, and not CBP, is essential for ionizing radiation-induced accumulation of the p53 tumor suppressor and thereby p53-mediated growth arrest. The results demonstrate that deficiency of p300 results in increased degradation of p53. Our findings suggest that p300 contributes to the stabilization and transactivation function of p53 in the cellular response to DNA damage.
Yuan
Z M
ZM
Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Huang
Y
Y
Ishiko
T
T
Nakada
S
S
Utsugisawa
T
T
Shioya
H
H
Utsugisawa
Y
Y
Yokoyama
K
K
Weichselbaum
R
R
Shi
Y
Y
Kufe
D
D
D050882:CREB-Binding Protein; D004249:DNA Damage; D006801:Humans; D009687:Nuclear Proteins / Q000378:metabolism*; D015534:Trans-Activators / Q000378:metabolism*; D015533:Transcriptional Activation / Q000528:radiation effects; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
D009687:Nuclear Proteins; D015534:Trans-Activators; D016159:Tumor Suppressor Protein p53; D050882:CREB-Binding Protein; C494363:CREBBP protein, human