Silencing of both β-TrCP1 and HOS (β-TrCP2) Is Required To Suppress Human Immunodeficiency Virus Type 1 Vpu-Mediated CD4 Down-Modulation-Reference-Cited by-同舟云学术

Silencing of both β-TrCP1 and HOS (β-TrCP2) Is Required To Suppress Human Immunodeficiency Virus Type 1 Vpu-Mediated CD4 Down-Modulation

Published:2007-02 Issue:3 Volume:81 Page:1502-1505
ISSN:0022-538X
Container-title:Journal of Virology
language:en
Short-container-title:J Virol

Author:

Butticaz Christophe¹,Michielin Olivier²³⁴,Wyniger Josiane¹,Telenti Amalio¹,Rothenberger Sylvia¹

Affiliation:

1. Institute of Microbiology, University Hospital of Lausanne, Lausanne, Switzerland

2. Multidisciplinary Oncology Center, University Hospital of Lausanne, Lausanne, Switzerland

3. Ludwig Institute for Cancer Research, Lausanne Branch, Lausanne, Switzerland

4. Swiss Institute of Bioinformatics, Epalinges, Switzerland

Abstract

ABSTRACT 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 β-TrCP1. Mammals possess a homologue of β-TrCP1, HOS, which is also named β-TrCP2. We show by coimmunoprecipitation experiments that β-TrCP2 binds Vpu and is able to induce CD4 down-modulation as efficiently as β-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 β-TrCP1 or β-TrCP2 but instead required the two genes to be silenced simultaneously.

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

Link

https://journals.asm.org/doi/pdf/10.1128/JVI.01711-06

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