DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Nari | ko |
dc.contributor.author | Kim, Min-Jung | ko |
dc.contributor.author | Sung, Pil Soo | ko |
dc.contributor.author | Bae, Yong Chul | ko |
dc.contributor.author | Shin, Eui-Cheol | ko |
dc.contributor.author | Yoo, Joo-Yeon | ko |
dc.date.accessioned | 2016-06-28T02:00:32Z | - |
dc.date.available | 2016-06-28T02:00:32Z | - |
dc.date.created | 2016-03-21 | - |
dc.date.created | 2016-03-21 | - |
dc.date.issued | 2016-02 | - |
dc.identifier.citation | NATURE COMMUNICATIONS, v.7 | - |
dc.identifier.issn | 2041-1723 | - |
dc.identifier.uri | http://hdl.handle.net/10203/207952 | - |
dc.description.abstract | Hepatitis C virus (HCV) utilizes autophagy to promote its propagation. Here we show the autophagy-mediated suppression of HCV replication via the endoplasmic reticulum (ER) protein SCOTIN. SCOTIN overexpression inhibits HCV replication and infectious virion production in cells infected with cell culture-derived HCV. HCV nonstructural 5A (NS5A) protein, which is a critical factor for HCV RNA replication, interacts with the IFN-beta-inducible protein SCOTIN, which transports NS5A to autophagosomes for degradation. Furthermore, the suppressive effect of SCOTIN on HCV replication is impaired in both ATG7-silenced cells and cells treated with autophagy or lysosomal inhibitors. SCOTIN does not affect the overall flow of autophagy; however, it is a substrate for autophagic degradation. The physical association between the transmembrane/proline-rich domain (TMPRD) of SCOTIN and Domain-II of NS5A is essential for autophagosomal trafficking and NS5A degradation. Altogether, our findings suggest that IFN-beta-induced SCOTIN recruits the HCV NS5A protein to autophagosomes for degradation, thereby restricting HCV replication. | - |
dc.language | English | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | HEPATITIS-C VIRUS | - |
dc.subject | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject | HEPATOMA-CELL LINE | - |
dc.subject | AUTOPHAGY MACHINERY | - |
dc.subject | IN-VITRO | - |
dc.subject | INFECTION | - |
dc.subject | MEMBRANE | - |
dc.subject | PARTICLES | - |
dc.subject | APOPTOSIS | - |
dc.subject | IMMUNITY | - |
dc.title | Interferon-inducible protein SCOTIN interferes with HCV replication through the autolysosomal degradation of NS5A | - |
dc.type | Article | - |
dc.identifier.wosid | 000371020200020 | - |
dc.identifier.scopusid | 2-s2.0-84958092750 | - |
dc.type.rims | ART | - |
dc.citation.volume | 7 | - |
dc.citation.publicationname | NATURE COMMUNICATIONS | - |
dc.identifier.doi | 10.1038/ncomms10631 | - |
dc.contributor.localauthor | Shin, Eui-Cheol | - |
dc.contributor.nonIdAuthor | Kim, Nari | - |
dc.contributor.nonIdAuthor | Kim, Min-Jung | - |
dc.contributor.nonIdAuthor | Bae, Yong Chul | - |
dc.contributor.nonIdAuthor | Yoo, Joo-Yeon | - |
dc.description.isOpenAccess | Y | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | HEPATITIS-C VIRUS | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | HEPATOMA-CELL LINE | - |
dc.subject.keywordPlus | AUTOPHAGY MACHINERY | - |
dc.subject.keywordPlus | IN-VITRO | - |
dc.subject.keywordPlus | INFECTION | - |
dc.subject.keywordPlus | MEMBRANE | - |
dc.subject.keywordPlus | PARTICLES | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | IMMUNITY | - |
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