Autoubiquitination of TRIM26 links TBK1 to NEMO in RLR-mediated innate antiviral immune response

作     者：Yong Ran Jing Zhang Li-Li Liu Zhao-Yi Pan Ying Nie Hong-Yan Zhang Yan-Yi Wang 

作者机构：Wuhan Institute of VirologyState Key Laboratory of VirologyChinese Academy of SciencesWuhan 430072China College of Life SciencesWuhan UniversityWuhan 430072China 

出 版 物：《Journal of Molecular Cell Biology》 (分子细胞生物学报（英文版）)

年 卷 期：2016年第8卷第1期

页      面：31-43页

核心收录：

学科分类：0906[农学-兽医学] 09[农学] 

基　　金：supported by the Ministry of Science and Technology of China(2014CB542603,2015CB554302) the National Natural Science Foundation of China(31425010,31321001,31270932,31170792,31400742) the 10000 Talents Plan,and the WIV‘One-Three-Five’Strategic Programs 

主　　题：TRIM26 TBK1 NEMO ubiquitination antiviral response 

摘      要：The transcription factors IRF3 and NF-kB are required for the expression of many genes involved in antiviral innate immune response,including type I interferons(IFNs)and proinflammatory *** is well established thatTBK1 isan essential kinase engageddownstream of multiple pattern-recognition receptors(PRRs)to mediate IRF3 phosphorylation and activation,whereas the precise mechanisms of TBK1 activation have not been fully elucidated ***,weidentified tripartite motif 26(TRIM26)as an important regulator for RNAvirus-triggered innate immune *** of TRIM26 impaired virus-triggered IRF3,NF-kB activation,IFN-b induction,and cellular antiviral ***26 was physically associated with TBK1 independent of viral *** an E3 ligase,TRIM26 underwent autoubiquitination upon viral *** TRIM26 subsequently associated with NEMO,thus bridging TBK1–NEMOinteraction,which is critical for the recruitment of TBK1 to the VISA signalsome and activation of *** findings suggest that TRIM26 is an important regulator of innate immune responses against RNA viruses,which functions by bridging TBK1 to NEMO and mediating the activation of TBK1.