Simian virus 40 large-T bypasses the translational block imposed by the phosphorylation of elF-2 alpha.
Simian virus 40 large-T bypasses the translational block imposed by the phosphorylation of elF-2 alpha.
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猿猴病毒 40 large-T 绕过 eF-2 α 磷酸化造成的翻译阻断。
DOI：
10.1006/viro.1996.0255
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发表时间：
1996
期刊：
影响因子：
3.7
通讯作者：
Thimmapaya,B
中科院分区：
文献类型：
--
作者：
Swaminathan,S;Rajan,P;Savinova,O;Jagus,R;Thimmapaya,B
抗病毒感染的细胞防御机制之一是通过激活干扰素诱导的双链RNA激活蛋白激酶PKR介导的。一旦激活，PKR磷酸化，从而使蛋白质合成起始因子eIF-2失活，导致蛋白质合成停止。病毒已经进化出不同的策略来抵消这种细胞抗病毒反应。这些策略中的大多数靶向PKR以防止其激活。最近，我们显示猴病毒40（SV 40）大T抗原在PKR活化的下游步骤逆转PKR介导的翻译抑制（Rajanet al.，69，785-795，1995）。在本文中，我们提出的证据表明，SV 40可以恢复有效的翻译细胞，尽管磷酸化的eIF-2α的水平升高导致PKR激活。因此，SV 40大T介导的翻译拯救发生在eIF-2α磷酸化的下游步骤。
One of the cellular defense mechanisms against virus infection is mediated by activating the interferon-induced, double-stranded-RNA-activated protein kinase, PKR. Upon activation, PKR phosphorylates and thereby inactivates the protein synthesis initiation factor, eIF-2, leading to cessation of protein synthesis. Viruses have evolved diverse strategies to counteract this cellular antiviral response. A majority of these strategies target PKR to prevent its activation. Recently, we showed that simian virus 40 (SV40) large-T antigen reverses PKR-mediated translational inhibition at a step downstream of PKR activation (Rajanet al., J. Virol.69, 785–795, 1995). In this paper, we present evidence showing that SV40 can restore efficient translation in cells despite the elevated levels of phosphorylated eIF-2α resulting from PKR activation. Thus, SV40 large-T-mediated translational rescue occurs at a step downstream of eIF-2α phosphorylation.