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내용필수	웹에디터 시작 > > > 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-b-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-b-induced SCOTIN recruits the HCV NS5A protein > to autophagosomes for degradation, thereby restricting HCV replication. > DOI: 10.1038/ncomms10631 OPEN > 1 > > 웹 에디터 끝
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