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TRIM29 negatively regulates p53 via inhibition of Tip60

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Title: TRIM29 negatively regulates p53 via inhibition of Tip60
Authors: Sho, Takuya Browse this author
Tsukiyama, Tadasuke Browse this author
Sato, Tomonobu Browse this author
Kondo, Takeshi Browse this author
Cheng, Jun Browse this author
Saku, Takashi Browse this author
Asaka, Masahiro Browse this author
Hatakeyama, Shigetsugu Browse this author
Keywords: TRIM29
p53
Tip60
Ubiquitin
Ataxia-telangiectasia
Issue Date: Jun-2011
Publisher: Elsevier B.V.
Journal Title: Biochimica et Biophysica Acta (BBA) : Molecular Cell Research
Volume: 1813
Issue: 6
Start Page: 1245
End Page: 1253
Publisher DOI: 10.1016/j.bbamcr.2011.03.018
PMID: 21463657
Abstract: 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. ATDC, 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.
Type: article (author version)
URI: http://hdl.handle.net/2115/46880
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 畠山 鎮次

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