TRIM11 binds to and destabilizes a key component of the activator-mediated cofactor complex (ARC105) through the ubiquitin-proteasome system

被引：32

作者：

Ishikawa, Hideaki ^{[1
]}

Tachikawa, Hiroyuki ^{[1
]}

Miura, Yutaka ^{[1
]}

Takahashi, Nobuhiro ^{[1
]}

机构：

[1] Tokyo Univ Agr & Technol, Dept Bioengn, United Grad Sch Agr, Fuchu, Tokyo 1838509, Japan

来源：

FEBS LETTERS | 2006年 / 580卷 / 20期

基金：

日本学术振兴会;

关键词：

TRIM/RBCC; ubiquitin-proteasome system; transcription mediator; TGF beta;

D O I：

10.1016/j.febslet.2006.07.066

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

TRIM11 is a member of the tripartite-motif-containing protein family and is known to destabilize humanin, an inhibitor of Alzheimer-like neuronal insults. In this study, we demonstrate that TRIM11 interacts with activator-recruited cofactor 105-kDa component (ARC105) that mediates chromatin-directed transcription activation and is a key regulatory factor for transforming growth factor P (TGFO) signaling. Coexpression of TRIM11 increased ARC105 degradation but a proteasome inhibitor suppressed this. Co-expression of TRIM11 and ARC105 also increased ubiquitination of ARC105. In addition, TRIM11 suppressed ARC105-mediated transcriptional activation induced with TGFO in a reporter assay. These results suggest that TRIM11, with the ubiquitin-proteasome pathway, regulates ARC105 function in TGF beta signaling. (c) 2006 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：4784 / 4792

页数：9

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