期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1813, 期 6, 页码 1245-1253出版社
ELSEVIER
DOI: 10.1016/j.bbamcr.2011.03.018
关键词
TRIM29; p53; Tip60; Ubiquitin; Ataxia-telangiectasia
资金
- Ministry of Education, Culture, Sports, Science and Technology
- Ono Cancer Research Fund
- The Ichiro Kanehara Foundation
- The Nakatomi Foundation
- Japan Brain Foundation
- Research Foundation Ituu Laboratory
- Grants-in-Aid for Scientific Research [21390087, 22390314, 23659144] Funding Source: KAKEN
Ataxia-telangiectasia (AT) is an autosomal recessive genetic disease characterized by immunological deficiencies, neurological degeneration, developmental abnormalities and an increased risk of cancer. Ataxia-telangiectasia group D (ATDC) was initially described as a gene related to AT. Ataxia-telangiectasia group D. also known as TRIM29, is structurally a member of the tripartite motif (TRIM) family of proteins, some of which have been reported to be highly expressed in some human carcinomas, but the involvement of TRIM29 in carcinogenesis has not been fully elucidated. In this study, we found by using yeast two-hybrid screening that TRIM29 binds to Tip60, which has been reported as a cellular acetyltransferase protein. Overexpression of TRIM29 promoted degradation and changed localization of Tip60 and reduced acetylation of p53 at lysine 120 by Tip60, resulting in enhancement of cell growth and transforming activity. In addition, we found that TRIM29 suppresses apoptosis induced by UV irradiation in HCT116 cell lines. These findings suggest that TRIM29 functions as an oncogene that promotes tumor growth. (C) 2011 Elsevier B.V. All rights reserved.
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