TRIM11 binds to and destabilizes a key component of the activator-mediated cofactor complex (ARC105) through the ubiquitin-proteasome system
TRIM11 binds to and destabilizes a key component of the activator-mediated cofactor complex (ARC105) through the ubiquitin-proteasome system
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DOI：
10.1016/j.febslet.2006.07.066
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发表时间：
2006-09-04
期刊：
影响因子：
3.5
通讯作者：
Takahashi, Nobuhiro
中科院分区：
文献类型：
--
作者：
Ishikawa, Hideaki;Tachikawa, Hiroyuki;Takahashi, Nobuhiro
TRIM 11是包含三部分基序的蛋白质家族的成员，并且已知使人蛋白（一种阿尔茨海默氏症样神经元损伤的抑制剂）不稳定。在这项研究中，我们证明了TRIM 11与激活剂募集辅因子105-kDa组分（ARC 105）相互作用，该组分介导染色质定向转录激活，并且是转化生长因子P（TGFO）信号传导的关键调节因子。TRIM 11的共表达增加了ARC 105的降解，但蛋白酶体抑制剂抑制了这一点。TRIM 11和ARC 105的共表达也增加了ARC 105的泛素化。此外，TRIM 11抑制ARC 105介导的转录激活诱导的TGFO在报告基因测定。这些结果表明，TRIM 11与泛素-蛋白酶体途径一起调节ARC 105在TGF β信号传导中的功能。(c)2006年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
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.