Suppr超能文献

紫外线DNA损伤修复结合蛋白的p127亚基(DDB1)对于副粘病毒猿猴病毒5的V蛋白靶向降解STAT1至关重要。

The p127 subunit (DDB1) of the UV-DNA damage repair binding protein is essential for the targeted degradation of STAT1 by the V protein of the paramyxovirus simian virus 5.

作者信息

Andrejeva J, Poole E, Young D F, Goodbourn S, Randall R E

机构信息

School of Biology, University of St. Andrews, Fife KY16 9TS, United Kingdom.

出版信息

J Virol. 2002 Nov;76(22):11379-86. doi: 10.1128/jvi.76.22.11379-11386.2002.

Abstract

The V protein of simian virus 5 (SV5) blocks interferon signaling by targeting STAT1 for proteasome-mediated degradation. Here we present three main pieces of evidence which demonstrate that the p127 subunit (DDB1) of the UV damage-specific DNA binding protein (DDB) plays a central role in this degradation process. First, the V protein of an SV5 mutant which fails to target STAT1 for degradation does not bind DDB1. Second, mutations in the N and C termini of V which abolish the binding of V to DDB1 also prevent V from blocking interferon (IFN) signaling. Third, treatment of HeLa/SV5-V cells, which constitutively express the V protein of SV5 and thus lack STAT1, with short interfering RNAs specific for DDB1 resulted in a reduction in DDB1 levels with a concomitant increase in STAT1 levels and a restoration of IFN signaling. Furthermore, STAT1 is degraded in GM02415 (2RO) cells, which have a mutation in DDB2 (the p48 subunit of DDB) which abolishes its ability to interact with DDB1, thereby demonstrating that the role of DDB1 in STAT1 degradation is independent of its association with DDB2. Evidence is also presented which demonstrates that STAT2 is required for the degradation of STAT1 by SV5. These results suggest that DDB1, STAT1, STAT2, and V may form part of a large multiprotein complex which leads to the targeted degradation of STAT1 by the proteasome.

摘要

猿猴病毒5(SV5)的V蛋白通过将信号转导子和转录激活子1(STAT1)靶向蛋白酶体介导的降解来阻断干扰素信号传导。在此,我们提供了三项主要证据,证明紫外线损伤特异性DNA结合蛋白(DDB)的p127亚基(DDB1)在这一降解过程中起核心作用。首先,一个无法将STAT1靶向降解的SV5突变体的V蛋白不与DDB1结合。其次,V蛋白N端和C端的突变消除了V与DDB1的结合,也阻止了V阻断干扰素(IFN)信号传导。第三,用针对DDB1的小干扰RNA处理组成性表达SV5的V蛋白因而缺乏STAT1的HeLa/SV5-V细胞,导致DDB1水平降低,同时STAT1水平升高,并且恢复了IFN信号传导。此外,STAT1在GM02415(2RO)细胞中被降解,这些细胞的DDB2(DDB的p48亚基)发生突变,消除了其与DDB1相互作用的能力,从而证明DDB1在STAT1降解中的作用独立于其与DDB2的关联。还提供了证据证明STAT2是SV5降解STAT1所必需的。这些结果表明,DDB1、STAT1、STAT2和V可能构成一个大型多蛋白复合物的一部分,该复合物导致蛋白酶体对STAT1进行靶向降解。

相似文献

引用本文的文献

本文引用的文献

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验