DDX5 inhibits type I IFN production by promoting degradation of TBK1 and disrupting formation of TBK1-TRAF3 complex
文献类型： 外文期刊
第一作者： Zhang, Yanwei
作者： Zhang, Yanwei;Cen, Jing;Yuan, Gaoliang;Jia, Zhao;Chen, Kangyong;Gao, Wa;Chen, Jing;Zou, Jun;Zhang, Yanwei;Cen, Jing;Yuan, Gaoliang;Jia, Zhao;Chen, Kangyong;Gao, Wa;Chen, Jing;Zou, Jun;Zhang, Yanwei;Cen, Jing;Yuan, Gaoliang;Jia, Zhao;Chen, Kangyong;Gao, Wa;Chen, Jing;Zou, Jun;Adamek, Mikolaj;Jia, Zhiying;Zou, Jun
作者机构：
关键词： PLAC8; CyHV3; SVCV; DDX5; TBK1; Autophagy
期刊名称：CELLULAR AND MOLECULAR LIFE SCIENCES （ 影响因子：8.0； 五年影响因子：8.7 ）
ISSN： 1420-682X
年卷期： 2023 年 80 卷 8 期
页码：
收录情况： SCI
摘要： DExD/H-box helicase (DDX) 5 belongs to the DExD/H-box helicase family. DDX family members play differential roles in the regulation of innate antiviral immune response. However, whether DDX5 is involved in antiviral immunity remains unclear. In this study, we found that DDX5 serves as a negative regulator of type I interferon (IFN) response. Overexpression of DDX5 inhibited IFN production induced by Spring viremia of carp virus (SVCV) and poly(I:C) and enhanced virus replication by targeting key elements of the RLR signaling pathway (MAVS, MITA, TBK1, IRF3 and IRF7). Mechanistically, DDX5 directly interacted with TBK1 to promote its autophagy-mediated degradation. Moreover, DDX5 was shown to block the interaction between TRAF3 and TBK1, hence preventing nuclear translocation of IRF3. Together, these data shed light on the roles of DDX5 in regulating IFN response.
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