Heat shock cognate 71 (HSC71) regulates cellular antiviral response by impairing formation of VISA aggregates  

作　　者：Zhigang Liu Shu-Wen Wu Cao-Qi Lei Qian Zhou Shu Li Hong-Bing Shu Yan-Yi Wang 

机构地区：[1]College of Life Sciences,Wuhan University,Wuhan 430072,China [2]Key Laboratory of Fermentation Engineering(Ministry of Education),Hubei University of Technology,Wuhan 430068,China [3]State Key Laboratory of Virology,Wuhan Institute of Virology,Chinese Academy of Sciences,Wuhan 430072,China

出　　处：《Protein & Cell》2013年第5期373-382,共10页蛋白质与细胞（英文版）

基　　金：supported by grants from the National Natural Science Foundation of China(Grant No.30921001,91029302,31000639 and 31170792);the National Basic Research Program(973 Program)(No.2012CB910201).

摘　　要：In response to viral infection, RIG-I-like RNA helicases detect viral RNA and signal through the mitochondrial adapter protein VISA. VISA activation leads to rapid activation of transcription factors IRF3 and NF-κB, which collaborate to induce transcription of type I interferon (IFN) genes and cellular antiviral response. It has been demonstrated that VISA is activated by forming prion-like aggregates. However, how this process is regulated remains unknown. Here we show that overexpression of HSC71 resulted in potent inhibition of virus-triggered transcription of IFNB1 gene and cellular antiviral response. Consistently, knockdown of HSC71 had opposite effects. HSC71 interacted with VISA, and negatively regulated virus-triggered VISA aggregation. These findings suggest that HSC71 functions as a check against VISA-mediated antiviral response.

关 键 词：HSC71 VISA Cellular antiviral response prion-like aggregate 

分 类 号：R51[医药卫生—内科学]