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J Biol Chem, Vol. 274, Issue 4, 1883-1886, January 22, 1999

COMMUNICATION
Role for p300 in Stabilization of p53 in the Response to DNA Damage

Zhi-Min Yuan, Yinyin Huang, Takatoshi Ishiko, Shuji Nakada, Taiju Utsugisawa, Hisashi Shioya, Yukari Utsugisawa, Kazunari Yokoyama, Ralph Weichselbaum^§, Yang Shi^¶, and Donald Kufe

From the Dana-Farber Cancer Institute and ^¶ Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, the  Tsukuba Life Science Center, The Institute of Physical and Chemical Research Koyadai, Tsukuba Science City 305, Japan, and the ^§ Department of Radiation and Cellular Oncology, University of Chicago, Chicago, Illinois 60637

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.

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Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.

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