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-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.
Electronic Supplementary Material
Supplementary material is available for this article at 10.1007/s13238-013-3902-3 and is accessible for authorized users.
Keywords: HSC71, VISA, Cellular antiviral response, prion-like aggregate
Electronic supplementary material
Footnotes
Electronic Supplementary Material
Supplementary material is available for this article at 10.1007/s13238-013-3902-3 and is accessible for authorized users.
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