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Hepatitis C virus p7 induces mitochondrial depolarization of isolated liver mitochondria

DC Field Value Language
dc.contributor.author김형중-
dc.date.accessioned2018-07-20T11:52:21Z-
dc.date.available2018-07-20T11:52:21Z-
dc.date.issued2017-
dc.identifier.issn1791-2997-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/161428-
dc.description.abstractHepatitis C virus (HCV)‑encoded protein p7 is a viroporin that acts as an ion channel and is indispensable for HCV particle production. Although the main target of HCV p7 is the endoplasmic reticulum, it also targets mitochondria. HCV‑infected cells show mitochondrial depolarization and ATP depletion; however, the function of HCV p7 in mitochondria is not fully understood. The present study demonstrated that treatment of isolated mouse liver mitochondria with the synthesized HCV p7 protein induced mitochondrial dysfunction. It also demonstrated that HCV p7 targeted isolated mouse liver mitochondria and induced mitochondrial depolarization. In addition, HCV p7 triggered matrix acidification and, ultimately, a decrease in ATP synthesis in isolated mitochondria. These findings indicate that targeting of mitochondria by HCV p7 in infected cells causes mitochondrial dysfunction to support HCV particle production. The present study provided evidence for the role of HCV p7 in mitochondria, and may lead to the development of novel strategies for HCV therapy.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherD. A. Spandidos-
dc.relation.isPartOfMOLECULAR MEDICINE REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleHepatitis C virus p7 induces mitochondrial depolarization of isolated liver mitochondria-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Internal Medicine-
dc.contributor.googleauthorYou Deok Gyun-
dc.contributor.googleauthorLee Hye Ra-
dc.contributor.googleauthorKim Won Ki-
dc.contributor.googleauthorKim Hyung Jung-
dc.contributor.googleauthorLee Gi Young-
dc.identifier.doi10.3892/mmr.2017.7809-
dc.contributor.localIdA01158-
dc.relation.journalcodeJ02261-
dc.identifier.eissn1791-3004-
dc.identifier.pmid29039530-
dc.identifier.urlhttps://search.proquest.com/docview/1986671164?accountid=15179-
dc.contributor.alternativeNameKim, Hyung Jung-
dc.contributor.affiliatedAuthorKim, Hyung Jung-
dc.citation.volume16-
dc.citation.number6-
dc.citation.startPage9533-
dc.citation.endPage9538-
dc.identifier.bibliographicCitationMOLECULAR MEDICINE REPORTS, Vol.16(6) : 9533-9538, 2017-
dc.identifier.rimsid61341-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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