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


ABSTRACT: 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-?B, 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.

SUBMITTER: Liu Z 

PROVIDER: S-EPMC4875550 | biostudies-literature | 2013 May

REPOSITORIES: biostudies-literature

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

Liu Zhigang Z   Wu Shu-Wen SW   Lei Cao-Qi CQ   Zhou Qian Q   Li Shu S   Shu Hong-Bing HB   Wang Yan-Yi YY  

Protein & cell 20130430 5


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 HS  ...[more]

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