TRAF7 negatively regulates the RLR signaling pathway by facilitating the K48-linked ubiquitination of TBK1

作     者：Jing-Ping Huang Ya-Xian Yang Tian Chen Dan-Dan Wang Jing Li Liang-Guo Xu Jing-Ping Huang;Ya-Xian Yang;Tian Chen;Dan-Dan Wang;Jing Li;Liang-Guo Xu

作者机构：College of Life ScienceJiangxi Normal UniversityNanchang330022China 

出 版 物：《Virologica Sinica》 (中国病毒学（英文版）)

年 卷 期：2023年第38卷第3期

页      面：419-428页

核心收录：

学科分类：1004[医学-公共卫生与预防医学(可授医学、理学学位)] 100401[医学-流行病与卫生统计学] 10[医学] 

基　　金：National Natural Science Foundation of China(Grant Nos.81971502 82060298 31570876) 

主　　题：TANK-Binding kinase 1(TBK1) Type I interferon TRAF7 Ubiquitination Innate immunity 

摘      要：TANK-binding kinase 1(TBK1)is a nodal protein involved in multiple signal transduction *** RNA virus-mediated innate immunity,TBK1 is recruited to the prion-like platform formed by MAVS and subsequently activates the transcription factors IRF3/7 and NF-κB to produce type I interferon(IFN)and proinflammatory cytokines for the signaling *** this study,TRAF7 was identified as a negative regulator of innate immune ***7 interacts with TBK1 and promotes K48-linked polyubiquitination and degradation of TBK1 through its RING domain,impairing the activation of IRF3 and the production of IFN-β.In addition,we found that the conserved cysteine residues at position 131 of TRAF7 are necessary for its function toward *** of TRAF7 could facilitate the activation of IRF3 and increase the transcript levels of downstream antiviral *** data suggest that TRAF7 negatively regulates innate antiviral immunity by promoting the K48-linked ubiquitination of TBK1.