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http://purl.uniprot.org/citations/28165510http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28165510http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28165510http://www.w3.org/2000/01/rdf-schema#comment"Type I interferons (IFNs) are multifunctional cytokines that regulate immune responses and cellular functions but also can have detrimental effects on human health. A tight regulatory network therefore controls IFN signaling, which in turn may interfere with medical interventions. The JAK-STAT signaling pathway transmits the IFN extracellular signal to the nucleus, thus resulting in alterations in gene expression. STAT2 is a well-known essential and specific positive effector of type I IFN signaling. Here, we report that STAT2 is also a previously unrecognized, crucial component of the USP18-mediated negative-feedback control in both human and mouse cells. We found that STAT2 recruits USP18 to the type I IFN receptor subunit IFNAR2 via its constitutive membrane-distal STAT2-binding site. This mechanistic coupling of effector and negative-feedback functions of STAT2 may provide novel strategies for treatment of IFN-signaling-related human diseases."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.org/dc/terms/identifier"doi:10.1038/nsmb.3378"xsd:string
http://purl.uniprot.org/citations/28165510http://purl.org/dc/terms/identifier"doi:10.1038/nsmb.3378"xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Li Z."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Li Z."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Zhang Y."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Piehler J."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Piehler J."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Fan J.B."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Fan J.B."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Yan M."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Yan M."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Heinisch J.J."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Heinisch J.J."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Colland F."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Colland F."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Zhang D.E."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Zhang D.E."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Miyauchi S."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Miyauchi S."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Pellegrini S."xsd:string
http://purl.uniprot.org/citations/28165510http://purl.uniprot.org/core/author"Pellegrini S."xsd:string