期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 479, 期 4, 页码 683-689出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.09.152
关键词
Hepatitis C virus; HCV; Golgi protein 73; GP73; Apolipoprotein E; ApoE; Hepatocellular carcinoma; HCC; Nonstructural protein 5A; NS5A; HCV particle assembly and secretion
资金
- Major State Basic Research Development Program (973 Program), Ministry of Science and Technology of the People's Republic of China [2012CB518900]
- National Natural Science Foundation of China [31230005, 81471942, 31270206, 31200134, 81171525]
- National Mega Project on Major Infectious Disease Prevention, National Health and Family Planning Commission of China [2012ZX10002006-003, 2012ZX10004-207]
- Chinese Foundation for Hepatitis Prevention and Control [CFHPC20132153]
Hepatitis C virus (HCV) infection is one of the leading causes of chronic liver diseases and hepatocellular carcinoma (HCC). Golgi protein 73 (GP73), a resident Golgi membrane protein, is a novel serum biomarker for the diagnosis of liver diseases and HCC. Although previous studies have demonstrated that HCV upregulates GP73 expression and GP73 promotes HCV secretion through its interaction with apolipoprotein E (ApoE), the exact mechanism underlying GP73 regulates HCV secretion remains unclear. In this study, we demonstrated that GP73 mediates the interaction of ApoE with HCV NS5A protein to promote HCV secretion. We revealed that GP73 is colocalized with HCV replication complex in infected-Huh7.5.1 cells. Further studies demonstrated that GP73 interacted with both NS5A and ApoE proteins. Furthermore, knockdown of GP73 significantly reduced the binding of NS5A with ApoE, and the production of virus particles in culture supernatant. Taken together, our studies revealed that GP73 promotes HCV secretion by directly mediating the interaction of ApoE with HCV replication complex through binding with HCV NS5A. (C) 2016 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据