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

Détails

ID Serval
serval:BIB_CDB1E001B3A9
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Silencing of both beta-TrCP1 and HOS (beta-TrCP2) is required to suppress human immunodeficiency virus type 1 Vpu-mediated CD4 down-modulation.
Périodique
Journal of virology
Auteur(s)
Butticaz C., Michielin O., Wyniger J., Telenti A., Rothenberger S.
ISSN
0022-538X
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
81
Numéro
3
Pages
1502150-5
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
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.
Mots-clé
Antigens, CD4/biosynthesis, Down-Regulation, Gene Expression Regulation, Viral, Gene Silencing/physiology, HIV-1/genetics, HIV-1/immunology, Hela Cells, Human Immunodeficiency Virus Proteins, Humans, T-Lymphocytes/immunology, T-Lymphocytes/virology, Ubiquitin-Protein Ligases/deficiency, Ubiquitin-Protein Ligases/genetics, Viral Regulatory and Accessory Proteins/physiology, beta-Transducin Repeat-Containing Proteins/deficiency, beta-Transducin Repeat-Containing Proteins/genetics
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/01/2008 12:22
Dernière modification de la notice
20/08/2019 16:48
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