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Recent evidence implicated the scaffold protein, 14-3-3, in Vpr cell cycle blockade.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>We found that in human T cells, 14-3-3 plays an active role in mediating Vpr-induced cell cycle arrest and reveal a dramatic increase in the amount of Cdk1, Cdc25C, and CyclinB1 bound to 14-3-3 \u03b8 during Vpr<jats:sub>v<\/jats:sub>-induced G<jats:sub>2<\/jats:sub>,M arrest. By contrast, a cell-cycle-arrest-dead Vpr mutant failed to augment 14-3-3 \u03b8 association with Cdk1 and CyclinB1. Moreover, G<jats:sub>2<\/jats:sub>,M arrest caused by HIV-1 infection strongly correlated with a disruption in 14-3-3 \u03b8 binding to centrosomal proteins, Plk1 and centrin. Finally, Vpr caused elevated levels of CyclinB1, Plk1, and Cdk1 in a complex with the nuclear transport and spindle assembly protein, importin \u03b2.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>Thus, our data reveal a new facet of Vpr-induced cell cycle arrest involving previously unrecognized abnormal rearrangements of multiprotein assemblies containing key cell cycle regulatory proteins.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Reviewers<\/jats:title>\n            <jats:p>This article was reviewed by David Kaplan, Nathaniel R. Landau and Yan Zhou.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1745-6150-3-17","type":"journal-article","created":{"date-parts":[[2008,4,29]],"date-time":"2008-04-29T18:13:49Z","timestamp":1209492829000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["14-3-3 theta binding to cell cycle regulatory factors is enhanced by HIV-1 Vpr"],"prefix":"10.1186","volume":"3","author":[{"given":"Diane L","family":"Bolton","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert A","family":"Barnitz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiko","family":"Sakai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J","family":"Lenardo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2008,4,29]]},"reference":[{"key":"95_CR1","doi-asserted-by":"publisher","first-page":"181","DOI":"10.1007\/BF01310474","volume":"120","author":"Y Nishino","year":"1991","unstructured":"Nishino Y, Kishi M, Sumiya M, Ogawa K, Adachi A, Maotani-Imai K, Kato S, Hirai K, Ikuta K: Human immunodeficiency virus type 1 vif, vpr, and vpu mutants can produce persistently infected cells. 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