SENP2 negatively regulates cellular antiviral response by deSUMOylating IRF3 and conditioning it for ubiquitination and degradation

作     者：Yong Ran Tian-Tian Liu Qian Zhou Shu Li Ai-Ping Mao Ying Li Li-Juan Liu Jin-Ke Cheng Hong-Bing Shu 

作者机构：College of Life SciencesWuhan UniversityWuhan 430072China Department of Biochemistry and Molecular Cell BiologySchool of MedicineShanghai Jiao Tong UniversityShanghai 200025China 

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

年 卷 期：2011年第3卷第5期

页      面：283-292页

核心收录：

学科分类：0710[理学-生物学] 071010[理学-生物化学与分子生物学] 081704[工学-应用化学] 07[理学] 08[工学] 0817[工学-化学工程与技术] 

基　　金：supported by the grants from the National Natural Science Foundation of China (30921001 and 91029302) 

主　　题：SENP2 IRF3 deSUMOylation ubiquitination innate immunity 

摘      要：Transcription factor IRF3-mediated type I interferon induction is essential for antiviral innate *** identified the deSUMOylating enzyme Sentrin/SUMO-specific protease(SENP)2 as a negative regulator of virus-triggered IFN-b *** of SENP2 caused IRF3 deSUMOylation,K48-linked ubiquitination,and degradation,whereas depletion of SENP2 had opposite *** the SUMOylation and K48-linked ubiquitination of IRF3 occurred at lysines 70 and 87,and these processes are *** level of virus-triggered IFN-b was markedly up-regulated and viral replication was reduced in SENP2-deficient cells comparing with wild-type *** findings suggest that SENP2 regulates antiviral innate immunity by deSUMOylating IRF3 and conditioning it for ubiquitination and degradation,and provide an example of cross-talk between the ubiquitin and SUMO pathways in innate immunity.