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Nonstructural 5A protein activates beta-catenin signaling cascades: implication of hepatitis C virus-induced liver pathogenesis.

DC Field Value Language
dc.contributor.author김호근-
dc.date.accessioned2015-04-24T17:29:51Z-
dc.date.available2015-04-24T17:29:51Z-
dc.date.issued2009-
dc.identifier.issn0168-8278-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/105510-
dc.description.abstractBACKGROUND/AIMS: The nonstructural 5A (NS5A) protein of hepatitis C virus (HCV) has been implicated in HCV-induced liver pathogenesis. Wnt/beta-catenin signaling has also been involved in tumorigenesis. To elucidate the molecular mechanism of HCV pathogenesis, we examined the potential effects of HCV NS5A protein on Wnt/beta-catenin signal transduction cascades. METHODS: The effects of NS5A protein on beta-catenin signaling cascades in hepatic cells were investigated by luciferase reporter gene assay, confocal microscopy, immunoprecipitation assay, and immunoblot analysis. RESULTS: beta-Catenin-mediated transcriptional activity is elevated by NS5A protein, in the context of HCV replication, and by infection of cell culture-produced HCV. NS5A protein directly interacts with endogenous beta-catenin and colocalizes with beta-catenin in the cytoplasm. NS5A protein inactivates glycogen synthase kinase 3beta and increases subsequent accumulation of beta-catenin in HepG2 cells. beta-Catenin was also accumulated in HCV patients' liver tissues. In addition, the accumulation of beta-catenin in HCV replicon cells requires both activation of phosphatidylinositol 3-kinase and inactivation of GSK3beta. CONCLUSIONS: NS5A activates beta-catenin signaling cascades through increasing the stability of beta-catenin. This modulation is accomplished by the protein interplay between viral and cellular signaling transducer. These data suggest that NS5A protein may directly be involved in Wnt/beta-catenin-mediated liver pathogenesis.-
dc.description.statementOfResponsibilityopen-
dc.format.extent853~864-
dc.relation.isPartOfJOURNAL OF HEPATOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHBasic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism-
dc.subject.MESHCOS Cells-
dc.subject.MESHCarcinoma, Hepatocellular/etiology-
dc.subject.MESHCarcinoma, Hepatocellular/metabolism-
dc.subject.MESHCarcinoma, Hepatocellular/virology-
dc.subject.MESHCell Line-
dc.subject.MESHCell Nucleus/metabolism-
dc.subject.MESHCercopithecus aethiops-
dc.subject.MESHCytosol/metabolism-
dc.subject.MESHGlycogen Synthase Kinase 3/antagonists & inhibitors-
dc.subject.MESHGlycogen Synthase Kinase 3/metabolism-
dc.subject.MESHGlycogen Synthase Kinase 3 beta-
dc.subject.MESHHepacivirus/genetics-
dc.subject.MESHHepacivirus/pathogenicity*-
dc.subject.MESHHepacivirus/physiology*-
dc.subject.MESHHumans-
dc.subject.MESHIn Vitro Techniques-
dc.subject.MESHLiver Neoplasms/etiology*-
dc.subject.MESHLiver Neoplasms/metabolism-
dc.subject.MESHLiver Neoplasms/virology-
dc.subject.MESHPhosphatidylinositol 3-Kinases/metabolism-
dc.subject.MESHProtein Interaction Domains and Motifs-
dc.subject.MESHRecombinant Proteins/genetics-
dc.subject.MESHRecombinant Proteins/metabolism-
dc.subject.MESHReplicon-
dc.subject.MESHSequence Deletion-
dc.subject.MESHSignal Transduction-
dc.subject.MESHTranscription Factor 4-
dc.subject.MESHTranscription Factors/metabolism-
dc.subject.MESHTransfection-
dc.subject.MESHViral Nonstructural Proteins/genetics-
dc.subject.MESHViral Nonstructural Proteins/metabolism*-
dc.subject.MESHVirus Replication-
dc.subject.MESHWnt Proteins/metabolism-
dc.subject.MESHbeta Catenin/chemistry-
dc.subject.MESHbeta Catenin/genetics-
dc.subject.MESHbeta Catenin/metabolism*-
dc.titleNonstructural 5A protein activates beta-catenin signaling cascades: implication of hepatitis C virus-induced liver pathogenesis.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학)-
dc.contributor.googleauthorChul-Yong Park-
dc.contributor.googleauthorSoo-Ho Choi-
dc.contributor.googleauthorSang-Min Kang-
dc.contributor.googleauthorJu-Il Kang-
dc.contributor.googleauthorByung-Yoon Ahn-
dc.contributor.googleauthorHoguen Kim-
dc.contributor.googleauthorGuhung Jung-
dc.contributor.googleauthorKang-Yell Choi-
dc.contributor.googleauthorSoon B. Hwang-
dc.identifier.doi10.1016/j.jhep.2009.06.026-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01183-
dc.relation.journalcodeJ01441-
dc.identifier.eissn1600-0641-
dc.identifier.pmid19726098-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0168827809005273-
dc.subject.keywordHepatitis C virus-
dc.subject.keywordLiver pathogenesis-
dc.subject.keywordNS5A protein-
dc.subject.keywordβ-Catenin signaling-
dc.subject.keywordTumorigenesis-
dc.contributor.alternativeNameKim, Ho Keun-
dc.contributor.affiliatedAuthorKim, Ho Keun-
dc.citation.volume51-
dc.citation.number5-
dc.citation.startPage853-
dc.citation.endPage864-
dc.identifier.bibliographicCitationJOURNAL OF HEPATOLOGY, Vol.51(5) : 853-864, 2009-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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