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c-Fos regulates hepatitis C virus propagation

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dc.contributor.authorKang, Sang-Min-
dc.contributor.authorLim, Seri-
dc.contributor.authorWon, Seung-Jae-
dc.contributor.authorShin, Ye-Jin-
dc.contributor.authorLim, Yun-Sook-
dc.contributor.authorAhn, Byung-Yoon-
dc.contributor.authorHwang, Soon B.-
dc.date.accessioned2021-09-07T07:05:35Z-
dc.date.available2021-09-07T07:05:35Z-
dc.date.created2021-06-18-
dc.date.issued2011-10-20-
dc.identifier.issn0014-5793-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/111358-
dc.description.abstractHepatitis C virus (HCV) RNA replication requires cellular factors as well as viral non-structural proteins (NS protein). Using small interfering RNA (siRNA) library screening, we previously identified c-Fos as a host factor involved in HCV propagation. In the present study, we demonstrated that silencing of c-Fos expression resulted in decrease of HCV propagation in cell culture grown HCV (HCVcc)-infected cells; whereas overexpression of c-Fos significantly increased HCV propagation. We further confirmed the positive role of c-Fos in HCV propagation by both HCV-luciferase reporter assay and immunofluorescence analysis. We showed that c-Fos level was upregulated by HCV infection. Furthermore, phorbol 12-myristate 13-acetate (PMA)-induced c-Fos level was synergistically increased by HCV infection. These data suggest that c-Fos acts as a positive regulator of HCV propagation and may contribute to HCV-associated pathogenesis. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherELSEVIER SCIENCE BV-
dc.subjectRNA REPLICATION COMPLEX-
dc.subjectVIRAL REPLICATION-
dc.subjectPROTEIN-
dc.subjectNS5A-
dc.subjectKINASE-
dc.subjectAP-1-
dc.subjectJUN-
dc.subjectTRANSCRIPTION-
dc.subjectACTIVATION-
dc.subjectEXPRESSION-
dc.titlec-Fos regulates hepatitis C virus propagation-
dc.typeArticle-
dc.contributor.affiliatedAuthorAhn, Byung-Yoon-
dc.identifier.doi10.1016/j.febslet.2011.08.041-
dc.identifier.scopusid2-s2.0-80054064329-
dc.identifier.wosid000296514100014-
dc.identifier.bibliographicCitationFEBS LETTERS, v.585, no.20, pp.3236 - 3244-
dc.relation.isPartOfFEBS LETTERS-
dc.citation.titleFEBS LETTERS-
dc.citation.volume585-
dc.citation.number20-
dc.citation.startPage3236-
dc.citation.endPage3244-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaBiophysics-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiophysics-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusRNA REPLICATION COMPLEX-
dc.subject.keywordPlusVIRAL REPLICATION-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusNS5A-
dc.subject.keywordPlusKINASE-
dc.subject.keywordPlusAP-1-
dc.subject.keywordPlusJUN-
dc.subject.keywordPlusTRANSCRIPTION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordAuthorHepatitis C virus-
dc.subject.keywordAuthorc-Fos-
dc.subject.keywordAuthorCellular factor-
dc.subject.keywordAuthorPropagation-
dc.subject.keywordAuthorPathogenesis-
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