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ORF2 protein of porcine circovirus type 2 promotes phagocytic activity of porcine macrophages by inhibiting proteasomal degradation of complement component 1, q subcomponent binding protein (C1QBP) through physical interaction

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dc.contributor.authorChoi, Chang-Yong-
dc.contributor.authorOh, Hae-Na-
dc.contributor.authorLee, Suk Jun-
dc.contributor.authorChun, Taehoon-
dc.date.accessioned2021-09-04T11:50:03Z-
dc.date.available2021-09-04T11:50:03Z-
dc.date.created2021-06-18-
dc.date.issued2015-10-
dc.identifier.issn0022-1317-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/92246-
dc.description.abstractDefining how each ORF of porcine circovirus type 2 (PCV2) manipulates the host immune system may be helpful to understand the disease progression of post-weaning multisystemic wasting syndrome. In this study, we demonstrated a direct interaction between the PCV2 ORF2 and complement component 1, q subcomponent binding protein (C1QBP) within the cytoplasm of host macrophages. The physical interaction between PCV2 ORF2 and C1QBP inhibited ubiquitin-mediated proteasomal degradation of C1QBP in macrophages. Increased stability of C1QBP by the interaction with PCV2 ORF2 further enhanced the phagocytic activity of porcine macrophages through the phosphoinositol 3-kinase signalling pathway. This may explain the molecular basis of how PCV2 ORF2 enhances the phagocytic activity of host macrophages.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherSOC GENERAL MICROBIOLOGY-
dc.subjectPATHOGENESIS-
dc.subjectEXPRESSION-
dc.subjectINFECTION-
dc.subjectDISEASE-
dc.subjectIDENTIFICATION-
dc.subjectINVOLVEMENT-
dc.subjectINDUCTION-
dc.subjectVIRUS-
dc.subjectCELLS-
dc.subjectPIGS-
dc.titleORF2 protein of porcine circovirus type 2 promotes phagocytic activity of porcine macrophages by inhibiting proteasomal degradation of complement component 1, q subcomponent binding protein (C1QBP) through physical interaction-
dc.typeArticle-
dc.contributor.affiliatedAuthorChun, Taehoon-
dc.identifier.doi10.1099/jgv.0.000282-
dc.identifier.scopusid2-s2.0-84946847767-
dc.identifier.wosid000367206200012-
dc.identifier.bibliographicCitationJOURNAL OF GENERAL VIROLOGY, v.96, pp.3294 - 3301-
dc.relation.isPartOfJOURNAL OF GENERAL VIROLOGY-
dc.citation.titleJOURNAL OF GENERAL VIROLOGY-
dc.citation.volume96-
dc.citation.startPage3294-
dc.citation.endPage3301-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiotechnology & Applied Microbiology-
dc.relation.journalResearchAreaVirology-
dc.relation.journalWebOfScienceCategoryBiotechnology & Applied Microbiology-
dc.relation.journalWebOfScienceCategoryVirology-
dc.subject.keywordPlusPATHOGENESIS-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusINFECTION-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusIDENTIFICATION-
dc.subject.keywordPlusINVOLVEMENT-
dc.subject.keywordPlusINDUCTION-
dc.subject.keywordPlusVIRUS-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusPIGS-
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