Home LiteratureArticle Details
PMID: 9890940 Published · ppublish English Journal Article

Role for p300 in stabilization of p53 in the response to DNA damage.

The Journal of biological chemistry ·Vol. 274 ·No. 4 ·1999-01-22 ·Pages 1883-6

Yuan ZM, Huang Y, Ishiko T, Nakada S, Utsugisawa T, Shioya H, Utsugisawa Y, Yokoyama K, Weichselbaum R, Shi Y, Kufe D

Abstract

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.

MeSH Terms
CREB-Binding Protein DNA Damage Humans Nuclear Proteins/metabolism Trans-Activators/metabolism Transcriptional Activation/radiation effects Tumor Cells, Cultured Tumor Suppressor Protein p53/metabolism
Chemicals
Nuclear Proteins Trans-Activators Tumor Suppressor Protein p53 CREB-Binding Protein CREBBP protein, human
Authors & Affiliations
11 authors, click to expand affiliations / ORCID
Yuan Z M
Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.
Huang Y
Ishiko T
Nakada S
Utsugisawa T
Shioya H
Utsugisawa Y
Yokoyama K
Weichselbaum R
Shi Y
Kufe D
Article Info
Journal
The Journal of biological chemistry
Abbr.
J Biol Chem
ISSN
0021-9258
Published
1999-01-22
Pages
1883-6
Language
English
Region
United States
NLM ID
2985121R
Subset
IM
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: [email protected]