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pubmed-article:2014052pubmed:dateCreated1991-5-13lld:pubmed
pubmed-article:2014052pubmed:abstractTextA decline in the T-cell population usually marks the onset of progressive immunological disease in individuals infected with the human immunodeficiency virus (HIV). Because CD4+ cells help to coordinate efficient immune responses, some of the defects in the immune function in advanced cases of AIDS may be explained by the disappearance of these cells. Therefore, an understanding of the mechanisms used by HIV to induce the reduction of CD4+ cells is important. Here we use a Moloney murine leukaemia virus-based retroviral vector in order to express the nef gene of HIV-1 in three lymphocytic cell lines expressing CD4. In all cases we find that cell-surface CD4 expression is inversely related to nef expression. However, nef does not alter steady-state levels of CD4 RNA or CD4 protein. Also, nef can downregulate a CD4 triple mutant (Ser----Ala) that is neither phosphorylated nor down-regulated by phorbol esters, indicating that nef is acting by a different mechanism.lld:pubmed
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pubmed-article:2014052pubmed:authorpubmed-author:MillerA DADlld:pubmed
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pubmed-article:2014052pubmed:articleTitleSerine phosphorylation-independent downregulation of cell-surface CD4 by nef.lld:pubmed
pubmed-article:2014052pubmed:affiliationProgram in molecular Medicine, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.lld:pubmed
pubmed-article:2014052pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:2014052pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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