Silencing of both β-TrCP1 and HOS (β-TrCP2) is required to suppress human immunodeficiency virus type 1 Vpu-mediated CD4 down-modulation

被引：30

作者：

Butticaz, Christophe

Michielin, Olivier

Wyniger, Josiane

Telenti, Amalio ^{[1
]}

Rothenberger, Sylvia

机构：

[1] Univ Lausanne Hosp, Inst Microbiol, Lausanne, Switzerland

[2] Univ Lausanne Hosp, Multidisciplinary Oncol Ctr, Lausanne, Switzerland

[3] Ludwig Inst Canc Res, Lausanne Branch, Lausanne, Switzerland

[4] Swiss Inst Bioinformat, Epalinges, Switzerland

来源：

JOURNAL OF VIROLOGY | 2007年 / 81卷 / 03期

关键词：

D O I：

10.1128/JVI.01711-06

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

The human immunodeficiency virus type 1 (HIV-1) Vpu protein interacts with CD4 within the endoplasmic reticula of infected cells and targets CD4 for degradation through interaction with beta-TrCP1. Mammals possess a homologue of beta-TrCP1, HOS, which is also named beta-TrCP2. We show by coimmunoprecipitation experiments that beta-TrCP2 binds Vpu and is able to induce CD4 down-modulation as efficiently as beta-TrCP1. In two different cell lines, HeLa CD4(+) and Jurkat, Vpu-mediated CD4 down-modulation could not be reversed through the individual silencing of endogenous beta-TrCP1 or beta-TrCP2 but instead required the two genes to be silenced simultaneously.

引用

页码：1502 / 1505

页数：4

共 26 条

[1] The human immunodeficiency virus type 1 accessory protein Vpu induces apoptosis by suppressing the nuclear factor κB-dependent expression of antiapoptotic factors [J].