单纯疱疹病毒1型Us11蛋白对PACT介导的PKR激活的抑制作用。
Inhibition of PACT-mediated activation of PKR by the herpes simplex virus type 1 Us11 protein.
作者信息
Peters Gregory A, Khoo David, Mohr Ian, Sen Ganes C
机构信息
Department of Molecular Biology, Lerner Research Institute, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
出版信息
J Virol. 2002 Nov;76(21):11054-64. doi: 10.1128/jvi.76.21.11054-11064.2002.
Abstract
PACT, a protein activator of PKR, can cause inhibition of cellular protein synthesis and apoptosis. Here, we report that the Us11 protein of herpes simplex virus type 1 can block PKR activation by PACT both in vitro and in vivo. Although Us11 can bind to both PKR and PACT, mutational analyses revealed that the binding of Us11 to PKR, and not to PACT, was essential for its inhibitory action. Similar analyses also revealed that the inhibitory effect was mediated by an interaction between the C-terminal half of Us11 and the N-terminal domain of PKR. The binding of Us11 to PKR did not block the binding of PKR to PACT but prevented its activation. Us11 is the first example of a viral protein that can inhibit the action of PACT on PKR.
摘要
PACT是蛋白激酶R（PKR）的一种蛋白激活剂，可导致细胞蛋白质合成抑制和细胞凋亡。在此，我们报告1型单纯疱疹病毒的Us11蛋白在体外和体内均可阻断PACT对PKR的激活作用。虽然Us11可与PKR和PACT都结合，但突变分析表明，Us11与PKR而非PACT的结合对其抑制作用至关重要。类似分析还表明，抑制作用是由Us11的C端后半部分与PKR的N端结构域之间的相互作用介导的。Us11与PKR的结合并未阻断PKR与PACT的结合，但阻止了PKR的激活。Us11是能抑制PACT对PKR作用的首个病毒蛋白实例。
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The herpes simplex virus type 1 U(S)11 protein interacts with protein kinase R in infected cells and requires a 30-amino-acid sequence adjacent to a kinase substrate domain.1型单纯疱疹病毒的U(S)11蛋白在受感染细胞中与蛋白激酶R相互作用，并且需要一个与激酶底物结构域相邻的30个氨基酸的序列。
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