巨细胞病毒M45抑制细胞死亡需要受体相互作用蛋白（RIP）同型相互作用基序（RHIM）依赖的与RIP1的相互作用。
Cytomegalovirus M45 cell death suppression requires receptor-interacting protein (RIP) homotypic interaction motif (RHIM)-dependent interaction with RIP1.
作者信息
Upton Jason W, Kaiser William J, Mocarski Edward S
机构信息
Department of Microbiology and Immunology, Emory Vaccine Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
出版信息
J Biol Chem. 2008 Jun 20;283(25):16966-70. doi: 10.1074/jbc.C800051200. Epub 2008 Apr 28.
Abstract
Herpesviruses such as cytomegaloviruses encode functions that modulate the innate response in diverse ways to counteract host sensing and delay host clearance during infection. The murine cytomegalovirus M45 protein interacts with receptor-interacting protein (RIP) 1 and RIP3 via a RIP homotypic interaction motif. Cell death suppression by M45 requires RIP homotypic interaction motif-dependent interaction with RIP1. This interaction also underlies the cell tropism role of M45 in preventing premature death of endothelial cells during murine cytomegalovirus infection. Thus, M45 is a viral inhibitor of RIP activation that provides a direct cell type-dependent replication benefit to the virus while modulating other biological processes signaling via the RIP1 adaptor such as activation of Toll-like receptor (TLR)3 as well as other mediators of cell death.
摘要
巨细胞病毒等疱疹病毒编码的功能可通过多种方式调节先天性免疫反应，以对抗宿主的感知并在感染期间延迟宿主的清除。小鼠巨细胞病毒M45蛋白通过RIP同型相互作用基序与受体相互作用蛋白（RIP）1和RIP3相互作用。M45对细胞死亡的抑制需要RIP同型相互作用基序依赖的与RIP1的相互作用。这种相互作用也是M45在小鼠巨细胞病毒感染期间防止内皮细胞过早死亡的细胞嗜性作用的基础。因此，M45是RIP激活的病毒抑制剂，它在调节通过RIP1衔接蛋白发出信号的其他生物学过程（如Toll样受体（TLR）3的激活以及细胞死亡的其他介质）的同时，为病毒提供了直接的细胞类型依赖性复制优势。
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