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http://purl.uniprot.org/citations/27777077http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27777077http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/27777077http://www.w3.org/2000/01/rdf-schema#comment"Interferon stimulated (sensitive) genes (ISGs) are the effector molecules downstream of type I/III interferon (IFN) signaling pathways in host innate immunity. ISG12a can be induced by IFN-α. Although ISG12a has been reported to inhibit the replication of HCV, the exact mechanism remains to be determined. In this study, we investigated the possible mechanisms of ISG12a anti-HCV property by exploring the production of type I IFN and the activation of Janus kinase/signal transducer and activator of transcription (Jak/STAT) signaling pathway, apoptosis and autophagy in Huh7.5.1 cells transiently transfected with ISG12a over-expression plasmid. Interestingly, we found that ISG12a inhibited HCV replication in both Con1b replicon and the HCV JFH1-based cell culture system and potentiated the anti-HCV activity of IFN-α. ISG12a promoted the production of IFN α/β and activated the type I IFN signaling pathway as shown by increased p-STAT1 level, higher Interferon sensitive response element (ISRE) activity and up-regulated ISG levels. However, ISG12a over-expression did not affect cell autophagy and apoptosis. Data from our current study collectively indicated that ISG12a inhibited HCV replication and potentiated the anti-HCV activity of IFN-α possibly through induced production of type I IFNs and activation of Jak/STAT signaling pathway independent of autophagy and cell apoptosis."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.org/dc/terms/identifier"doi:10.1016/j.virusres.2016.10.013"xsd:string
http://purl.uniprot.org/citations/27777077http://purl.org/dc/terms/identifier"doi:10.1016/j.virusres.2016.10.013"xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Chen L."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Chen L."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Li S."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Shi X."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Shi X."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Yao M."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Yao M."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Zheng Z."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Zheng Z."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Jiao B."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/author"Jiao B."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/name"Virus Res."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/name"Virus Res."xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/pages"231-239"xsd:string
http://purl.uniprot.org/citations/27777077http://purl.uniprot.org/core/pages"231-239"xsd:string