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. 2013 Apr 30;4(5):373–382. doi: 10.1007/s13238-013-3902-3

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

Zhigang Liu 13902,23902, Shu-Wen Wu 13902, Cao-Qi Lei 13902, Qian Zhou 13902, Shu Li 13902, Hong-Bing Shu 13902, Yan-Yi Wang 13902,33902,
PMCID: PMC4875550  PMID: 23636689

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

13238_2013_3902_MOESM1_ESM.pdf (83.5KB, pdf)

Supplementary material, approximately 83.5 KB.

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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Supplementary Materials

13238_2013_3902_MOESM1_ESM.pdf (83.5KB, pdf)

Supplementary material, approximately 83.5 KB.


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