| Autor: |
Butticaz C; Institute of Microbiology, University Hospital of Lausanne, Lausanne, Switzerland., Michielin O, Wyniger J, Telenti A, Rothenberger S |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of virology [J Virol] 2007 Feb; Vol. 81 (3), pp. 1502-5. Date of Electronic Publication: 2006 Nov 22. |
| DOI: |
10.1128/JVI.01711-06 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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