PKR-dependent mechanisms of interferon-alpha for inhibiting hepatitis B virus replication
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park, Il-Hyun | - |
dc.contributor.author | Baek, Kyung-Won | - |
dc.contributor.author | Cho, Eun-Young | - |
dc.contributor.author | Ahn, Byung-Yoon | - |
dc.date.accessioned | 2021-09-07T09:49:55Z | - |
dc.date.available | 2021-09-07T09:49:55Z | - |
dc.date.created | 2021-06-19 | - |
dc.date.issued | 2011-08 | - |
dc.identifier.issn | 1016-8478 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/111866 | - |
dc.description.abstract | Interferon-alpha (IFN-alpha) inhibits the replication of hepatitis B virus (HBV) in vivo and in vitro, but the molecular mechanism of this inhibition has been elusive. We found that while HBV replication in transfected human hepatoma Huh-7 cell was severely inhibited by IFN-alpha treatment as reported previously, this inhibition was markedly impaired in the cell in which the expression of IFN-inducible, double-stranded RNA-dependent protein kinase (PKR) was stably and specifically suppressed through RNA-interference. Intracellular level of viral capsids was down-regulated likewise in a PKR-dependent manner, whereas that of HBV transcripts including the viral RNA pregenome was not affected by IFN-alpha treatment. Ectopic expression of PKR also resulted in the reduction of viral capsids with concomitant increase of phosphorylated eIF2 alpha. These results suggested that PKR functions as a key mediator of IFN-alpha in opposing HBV replication, most likely through the inhibition of protein synthesis. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | KOREAN SOC MOLECULAR & CELLULAR BIOLOGY | - |
dc.subject | HUMAN HEPATOMA-CELLS | - |
dc.subject | GENE-EXPRESSION | - |
dc.subject | TRANSGENIC MICE | - |
dc.subject | PROTEIN | - |
dc.subject | RNA | - |
dc.subject | NUCLEOCAPSIDS | - |
dc.subject | ACTIVATION | - |
dc.subject | DNA | - |
dc.title | PKR-dependent mechanisms of interferon-alpha for inhibiting hepatitis B virus replication | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Ahn, Byung-Yoon | - |
dc.identifier.doi | 10.1007/s10059-011-1059-6 | - |
dc.identifier.scopusid | 2-s2.0-81055157995 | - |
dc.identifier.wosid | 000294475300007 | - |
dc.identifier.bibliographicCitation | MOLECULES AND CELLS, v.32, no.2, pp.167 - 172 | - |
dc.relation.isPartOf | MOLECULES AND CELLS | - |
dc.citation.title | MOLECULES AND CELLS | - |
dc.citation.volume | 32 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 167 | - |
dc.citation.endPage | 172 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.identifier.kciid | ART001577548 | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | HUMAN HEPATOMA-CELLS | - |
dc.subject.keywordPlus | GENE-EXPRESSION | - |
dc.subject.keywordPlus | TRANSGENIC MICE | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | RNA | - |
dc.subject.keywordPlus | NUCLEOCAPSIDS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | DNA | - |
dc.subject.keywordAuthor | antiviral mechanism | - |
dc.subject.keywordAuthor | Hepatitis B virus | - |
dc.subject.keywordAuthor | IFN-alpha | - |
dc.subject.keywordAuthor | PKR | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
145 Anam-ro, Seongbuk-gu, Seoul, 02841, Korea+82-2-3290-2963
COPYRIGHT © 2021 Korea University. All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.