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Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317.

Bolduan, Sebastian ; Votteler, Jörg ; Lodermeyer, Veronika ; Greiner, Timo ; Koppensteiner, Herwig ; Schindler, Michael ; Thiel, Gerhard ; Schubert, Ulrich (2011)
Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317.
In: Virology, 416 (1-2)
Artikel, Bibliographie

Kurzbeschreibung (Abstract)

While the C-terminal domain of HIV-1 Vpu is critical for CD4 degradation, the transmembrane domain (TM) mediates ion channel activity, enhances virus release and is essential for counteracting CD317/Bst-2/Tetherin. Here we analyzed whether the ion channel activity of Vpu is required to antagonize CD317-mediated restriction of virion release. We examined TM-mutants of three conserved residues: the S23A mutation, which was previously shown to abrogate ion channel function, did not affect Vpu mediated augmentation of virus release. In contrast, the A14N and A18N mutation did not affect ion channel activity of Vpu, but substantially reduced its ability to support virus release and to down-regulate CD317 from the cell surface. Altogether, our data suggest that not the ion channel activity of Vpu, but its ability to remove CD317 from the cell surface is required to augment HIV-1 release.

Typ des Eintrags: Artikel
Erschienen: 2011
Autor(en): Bolduan, Sebastian ; Votteler, Jörg ; Lodermeyer, Veronika ; Greiner, Timo ; Koppensteiner, Herwig ; Schindler, Michael ; Thiel, Gerhard ; Schubert, Ulrich
Art des Eintrags: Bibliographie
Titel: Ion channel activity of HIV-1 Vpu is dispensable for counteraction of CD317.
Sprache: Englisch
Publikationsjahr: 2011
Titel der Zeitschrift, Zeitung oder Schriftenreihe: Virology
Jahrgang/Volume einer Zeitschrift: 416
(Heft-)Nummer: 1-2
Kurzbeschreibung (Abstract):

While the C-terminal domain of HIV-1 Vpu is critical for CD4 degradation, the transmembrane domain (TM) mediates ion channel activity, enhances virus release and is essential for counteracting CD317/Bst-2/Tetherin. Here we analyzed whether the ion channel activity of Vpu is required to antagonize CD317-mediated restriction of virion release. We examined TM-mutants of three conserved residues: the S23A mutation, which was previously shown to abrogate ion channel function, did not affect Vpu mediated augmentation of virus release. In contrast, the A14N and A18N mutation did not affect ion channel activity of Vpu, but substantially reduced its ability to support virus release and to down-regulate CD317 from the cell surface. Altogether, our data suggest that not the ion channel activity of Vpu, but its ability to remove CD317 from the cell surface is required to augment HIV-1 release.

Fachbereich(e)/-gebiet(e): 10 Fachbereich Biologie > Plant Membrane Biophyscis (am 20.12.23 umbenannt in Biologie der Algen und Protozoen)
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10 Fachbereich Biologie
Hinterlegungsdatum: 21 Jun 2011 11:52
Letzte Änderung: 05 Mär 2013 09:49
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