| http://purl.uniprot.org/citations/21310048 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21310048 | http://www.w3.org/2000/01/rdf-schema#comment | "BackgroundThe cellular transmembrane protein CD317/BST-2/HM1.24/Tetherin restricts HIV-1 infection by physically tethering mature virions to the surface of infected cells. HIV-1 counteracts this restriction by expressing the accessory protein Vpu, yet the mechanism of this antagonism is incompletely understood. β-TrCP is the substrate recognition domain of an E3 ubiquitin ligase complex that interacts with the di-serine motif S52/S56 in the cytoplasmic tail of Vpu to target the CD4 receptor for proteasomal degradation. Recently, it has been suggested that β-TrCP is also critically involved in Vpu's ability to overcome the CD317-mediated virion release block.ResultsTo test this model, we analyzed the consequences of several experimental strategies to interfere with the Vpu-β-TrCP protein-protein interaction. Under these conditions, we studied effects of Vpu on expression and localization of CD317 and CD4, as well as on its ability to promote HIV-1 release. Our results demonstrate a strict requirement for Vpu's di-serine motif for degradation of CD4 and also CD317, reduction of cell surface exposure of CD317, and HIV-1 release enhancement. We further show a critical role of β-TrCP2, but not of the structurally related β-TrCP1 isoform, for Vpu-mediated degradation of both receptors. Most importantly, Vpu remained active in downregulating CD317 from the cell surface and in overcoming the HIV-1 release restriction in β-TrCP-depleted cells.ConclusionsThese results demonstrate that β-TrCP is not strictly required for Vpu's ability to counteract the CD317-imposed virion release block and support the relevance of cell surface down-modulation of the restriction factor as a central mechanism of Vpu antagonism. Moreover, we propose the existence of a critical, yet to be identified cellular factor that interacts with Vpu via its di-serine motif to alter the trafficking of the restriction factor."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.org/dc/terms/identifier | "doi:10.1186/1742-4690-8-9"xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/author | "Fackler O.T."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/author | "Keppler O.T."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/author | "Homann S."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/author | "Tervo H.M."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/author | "Ambiel I."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/author | "Fritz J.V."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/name | "Retrovirology"xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/pages | "9"xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/title | "beta-TrCP is dispensable for Vpu's ability to overcome the CD317/Tetherin-imposed restriction to HIV-1 release."xsd:string |
| http://purl.uniprot.org/citations/21310048 | http://purl.uniprot.org/core/volume | "8"xsd:string |
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