HIV‐1 auxiliary regulatory protein Vpr promotes ubiquitination and turnover of Vpr mutants containing the L64P mutation

FEBS Letters

Jian, Heng¹  Zhu, Henghu¹  Zhao, Ling-Jun¹ 

[1] Institute for Molecular Virology, St. Louis University School of Medicine, 3681 Park Avenue, St. Louis, MO 63110, USA

关键词: Vpr;    Turnover;    Ubiquitination;    Proteasome;    Apoptosis;    Subtype;   

DOI  :  10.1016/S0014-5793(04)00299-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The auxiliary regulatory protein Vpr of HIV-1 possesses several biological activities which are believed to facilitate HIV-1 replication and pathogenesis. In this report, experimental evidence suggests a novel biological activity of Vpr: facilitation of the turnover of Vpr mutants bearing the L64P mutation. This novel activity of Vpr was shared by Vpr molecules from different subtypes of HIV-1. Co-expression of the wild type Vpr with the VprW54A/L64P mutant resulted in normal synthesis of the mutant mRNA but enhanced ubiquitination and turnover of the mutant protein. These results suggest that Vpr may interact with the ubiquitin/proteasome pathway to regulate the stability of viral or cellular proteins.

【 授权许可】

Unknown