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http://purl.uniprot.org/citations/35878012http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35878012http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/35878012http://www.w3.org/2000/01/rdf-schema#comment"Viruses evade the innate immune response by suppressing the production or activity of cytokines such as type I interferons (IFNs). Here we report the discovery of a mechanism by which the SARS-CoV-2 virus coopts an intrinsic cellular machinery to suppress the production of the key immunostimulatory cytokine IFN-β. We reveal that the SARS-CoV-2 encoded nonstructural protein 2 (NSP2) directly interacts with the cellular GIGYF2 protein. This interaction enhances the binding of GIGYF2 to the mRNA cap-binding protein 4EHP, thereby repressing the translation of the Ifnb1 mRNA. Depletion of GIGYF2 or 4EHP significantly enhances IFN-β production, which inhibits SARS-CoV-2 replication. Our findings reveal a target for rescuing the antiviral innate immune response to SARS-CoV-2 and other RNA viruses."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.org/dc/terms/identifier"doi:10.1073/pnas.2204539119"xsd:string
http://purl.uniprot.org/citations/35878012http://purl.org/dc/terms/identifier"doi:10.1073/pnas.2204539119"xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Luo J."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Luo J."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Li Q."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Li Q."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Mao X."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Mao X."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Lin R."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Lin R."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Yang J."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Yang J."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Zhou L."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Zhou L."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Zhang C."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Zhang C."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Xu Z."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Xu Z."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Alain T."xsd:string
http://purl.uniprot.org/citations/35878012http://purl.uniprot.org/core/author"Alain T."xsd:string