SUMOylation of RIG-I positively regulates the type I interferon signaling

查看全文 作　　者：Zhiqiang [1,2]Mi;Jihuan [2]Fu;Yanbao [2]Xiong;Hong [2]Tang

机构地区：[1]Center for Molecular Immunology,Institute of Microbiology,Chinese Academy of Sciences,Beijing 100101,China;[2]Key Laboratory of Infection and Immunity of Chinese Academy of Sciences,Institute of Biophysics,Beijing 100101,China

出　　处：《Protein & Cell》索引2010年第1卷第3期,共9页

基　　金：grants from Chinese Academy of Sciences(Grant No.KSCX1-YW-10);the Ministry of Science and Technology(Grant Nos.2006CB910901,2007DFC30190,2008ZX10001-002 and 2009CB522506);H.T.The authors have no conflicting financial interests. 摘　　要：Retinoic acid-inducible gene-I(RIG-I)functions as an intracellular pattern recognition receptor(PRR)that recognizes the 5'-triphosphate moiety of single-stranded RNA viruses to initiate the innate immune response.Previous studies have shown that Lys63-linked ubiquitylation is required for RIG-I activation and the downstream anti-viral type I interferon(IFN-I)induction.Herein we reported that,RIG-I was also modified by small ubiquitin-like modifier-1(SUMO-1).Functional analysis showed that RIG-I SUMOylation enhanced IFN-I production through increased ubiquitylation and the interaction with its downstream adaptor molecule Cardif.Our results therefore suggested that SUMOylation might serve as an additional regulatory tier for RIG-I activation and IFN-I signaling. 关键词：RIG-I SUMOYLATION type I interferon innate immunity

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SUMOylation of RIG-I positively regulates the type I interferon signaling

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