Encephalomyocarditis virus 3C protease attenuates type I interferon production through disrupting the TANK-TBK1-IKK epsilon-IRF3 complex

文献类型： 外文期刊

第一作者： Huang, Li

作者： Huang, Li;Yu, Huibin;Zhang, Kunli;Li, Changyao;Hu, Liang;Zhang, Yuanfeng;Zhang, Lijie;Liu, Qinfang;Wang, Shengnan;He, Xijun;Bu, Zhigao;Cai, Xuehui;Li, Jiangnan;Weng, Changjiang;Xiong, Tao;Zhang, Quan;Cui, Shangjin

作者机构：

期刊名称：BIOCHEMICAL JOURNAL （ 影响因子：3.857； 五年影响因子：4.868 ）

ISSN：

年卷期：

页码：

收录情况： SCI

摘要： TRAF family member-associated NF-kappa B activator (TANK) is a scaffold protein that assembles into the interferon (IFN) regulator factor 3 (IRF3)-phosphorylating TANK-binding kinase 1 (TBK1)-(I kappa B) kinase epsilon (IKK epsilon) complex, where it is involved in regulating phosphorylation of the IRF3 and IFN production. However, the functions of TANK in encephalomyocarditis virus (EMCV) infection-induced type I IFN production are not fully understood. Here, we demonstrated that, instead of stimulating type I IFN production, the EMCV-HB10 strain infection potently inhibited Sendai virus-and polyI:C-induced IRF3 phosphorylation and type I IFN production in HEK293T cells. Mechanistically, EMCV 3C protease (EMCV 3C) cleaved TANK and disrupted the TANK-TBK1-IKK epsilon-IRF3 complex, which resulted in the reduction in IRF3 phosphorylation and type I IFN production. Taken together, our findings demonstrate that EMCV adopts a novel strategy to evade host innate immune responses through cleavage of TANK.

分类号： Q5

  • 相关文献
作者其他论文 更多>>

微信小程序