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Virus infection may induce excessive interferon (IFN) responses that can lead to host tissue injury or even death. β-arrestin 2 regulates multiple cellular events through the G protein-coupled receptor (GPCR) signaling pathways. Here we demonstrate that β-arrestin 2 also promotes virus-induced production of IFN-β and clearance of viruses in macrophages. β-arrestin 2 interacts with cyclic GMP-AMP synthase (cGAS) and increases the binding of dsDNA to cGAS to enhance cyclic GMP-AMP (cGAMP) production and the downstream stimulator of interferon genes (STING) and innate immune responses. Mechanistically, deacetylation of β-arrestin 2 at Lys171 facilitates the activation of the cGAS–STING signaling and the production of IFN-β. In vitro, viral infection induces the degradation of β-arrestin 2 to facilitate immune evasion, while a β-blocker, carvedilol, rescues β-arrestin 2 expression to maintain the antiviral immune response. Our results thus identify a viral immune-evasion pathway via the degradation of β-arrestin 2, and also hint that carvedilol, approved for treating heart failure, can potentially be repurposed as an antiviral drug candidate.
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?:doi
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10.1038/s41467-020-19849-9
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document_parses/pdf_json/1087ecf7c85b8ab165de9528b08e7c245094974c.json; document_parses/pdf_json/78dea52d3ca4f65230fc1f950b695d4b324a6c37.json; document_parses/pdf_json/1738f3f859ec70b28d4dfe62528346f77669d008.json
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document_parses/pmc_json/PMC7691508.xml.json
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β-arrestin 2 as an activator of cGAS-STING signaling and target of viral immune evasion
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