Induction of APOBEC3G ubiquitination and degradation by an HIV-1 Vif-Cul5-SCF complex

被引：992

作者：

Yu, XH

Yu, YK

Liu, BD

Luo, K

Kong, W

Mao, PY

Yu, XF ^{[1
]}

机构：

[1] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mol Microbiol & Immunol, Baltimore, MD 21205 USA

[2] Jilin Univ, Changchun, Peoples R China

[3] Zhejiang Univ, Hangzhou 310027, Peoples R China

来源：

SCIENCE | 2003年 / 302卷 / 5647期

关键词：

D O I：

10.1126/science.1089591

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Human immunodeficiency virus-1 (HIV-1) Vif is essential for viral evasion of host antiviral factor CEM15/APOBEC3G. We report that Vif interacts with cellular proteins Cul5, elongins B and C, and Rbx1 to form an Skp1-cullin-F-box (SCF)-like complex. The ability of Vif to suppress antiviral activity of APOBEC3G was specifically dependent on Cul5-SCF function, allowing Vif to interact with APOBEC3G and induce its ubiquitination and degradation. A Vif mutant that interacted with APOBEC3G but not with Cul5-SCF was functionally inactive. The Cul5-SCF was also required for Vif function in distantly related simian immunodeficiency virus mac. These results indicate that the conserved Cul5-SCF pathway used by Vif is a potential target for antiviral development.

引用

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页码：1056 / 1060

页数：5

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