{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360574096258671872.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1128/jvi.01650-07"}},{"identifier":{"@type":"URI","@value":"https://journals.asm.org/doi/pdf/10.1128/JVI.01650-07"}},{"identifier":{"@type":"PMID","@value":"18057259"}}],"dc:title":[{"@value":"Negative Feedback Regulation of RIG-I-Mediated Antiviral Signaling by Interferon-Induced ISG15 Conjugation"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>ABSTRACT</jats:title>\n          <jats:p>\n            RIG-I senses intracellular virus-specific nucleic acid structures and initiates an antiviral response that induces interferon (IFN) production, which, in turn, activates the transcription of RIG-I to increase RIG-I protein levels. Upon intracellular poly(I:C) stimulation, however, the levels of RIG-I protein did not correlate with the expression patterns of\n            <jats:italic>RIG-I</jats:italic>\n            transcripts. When the ISG15 conjugation system was overexpressed, ISG15 was conjugated to RIG-I and cellular levels of the unconjugated form of RIG-I decreased. The ISGylation of RIG-I reduced levels of both basal and virus-induced IFN promoter activity. Levels of unconjugated RIG-I also decreased when 26S proteasome activity was blocked by treatment with MG132, ALLN, or Lactacystin. In the presence of MG132, ISG15 conjugation to RIG-I increased, and hence, the unconjugated form of RIG-I was reduced. In Ube1L\n            <jats:sup>−/−</jats:sup>\n            cells, which lack the ability to conjugate ISG15, basal levels of both RIG-I protein and transcripts were increased compared to those in wild-type cells. As a result, enhanced production of ISGs and enhanced IFN promoter activity in Ube1L\n            <jats:sup>−/−</jats:sup>\n            cells were observed, and the phenotype was restored to that of wild-type cells by the overexpression of Ube1L. Based on these results, we propose a novel negative feedback loop which adjusts the strength of the RIG-I-mediated antiviral response and IFN production through the regulation of RIG-I protein by IFN-induced ISG15 conjugation.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380574096258671873","@type":"Researcher","foaf:name":[{"@value":"Min-Jung Kim"}],"jpcoar:affiliationName":[{"@value":"Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 790-784, Republic of Korea"}]},{"@id":"https://cir.nii.ac.jp/crid/1380574096258671875","@type":"Researcher","foaf:name":[{"@value":"Sun-Young Hwang"}],"jpcoar:affiliationName":[{"@value":"Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 790-784, Republic of Korea"}]},{"@id":"https://cir.nii.ac.jp/crid/1380574096258671872","@type":"Researcher","foaf:name":[{"@value":"Tadaatsu Imaizumi"}],"jpcoar:affiliationName":[{"@value":"Department of Vascular Biology, Hirosaki University School of Medicine, Hirosaki 036-8562, Japan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380574096258671874","@type":"Researcher","foaf:name":[{"@value":"Joo-Yeon Yoo"}],"jpcoar:affiliationName":[{"@value":"Department of Life Sciences, Pohang University of Science and Technology (POSTECH), Pohang 790-784, Republic of Korea"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"0022538X"},{"@type":"EISSN","@value":"10985514"}],"prism:publicationName":[{"@value":"Journal of Virology"}],"dc:publisher":[{"@value":"American Society for Microbiology"}],"prism:publicationDate":"2008-02","prism:volume":"82","prism:number":"3","prism:startingPage":"1474","prism:endingPage":"1483"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["https://journals.asm.org/non-commercial-tdm-license"],"url":[{"@id":"https://journals.asm.org/doi/pdf/10.1128/JVI.01650-07"}],"createdAt":"2007-12-06","modifiedAt":"2022-03-05","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Feedback,%20Physiological","dc:title":"Feedback, Physiological"},{"@id":"https://cir.nii.ac.jp/all?q=Ubiquitin-Activating%20Enzymes","dc:title":"Ubiquitin-Activating Enzymes"},{"@id":"https://cir.nii.ac.jp/all?q=Models,%20Biological","dc:title":"Models, Biological"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Line","dc:title":"Cell Line"},{"@id":"https://cir.nii.ac.jp/all?q=DEAD-box%20RNA%20Helicases","dc:title":"DEAD-box RNA Helicases"},{"@id":"https://cir.nii.ac.jp/all?q=Poly%20I-C","dc:title":"Poly I-C"},{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Expression%20Regulation","dc:title":"Gene Expression Regulation"},{"@id":"https://cir.nii.ac.jp/all?q=Viruses","dc:title":"Viruses"},{"@id":"https://cir.nii.ac.jp/all?q=Animals","dc:title":"Animals"},{"@id":"https://cir.nii.ac.jp/all?q=Cytokines","dc:title":"Cytokines"},{"@id":"https://cir.nii.ac.jp/all?q=DEAD%20Box%20Protein%2058","dc:title":"DEAD Box Protein 58"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Interferons","dc:title":"Interferons"},{"@id":"https://cir.nii.ac.jp/all?q=Receptors,%20Immunologic","dc:title":"Receptors, Immunologic"},{"@id":"https://cir.nii.ac.jp/all?q=Ubiquitins","dc:title":"Ubiquitins"}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050869456404541440","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"RIG-I triggers a signaling-abortive anti-SARS-CoV-2 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