Linked Life Data

11914580

Source:http://linkedlifedata.com/resource/pubmed/id/11914580

Statements in which the resource exists.
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pubmed-article:11914580pubmed:abstractTextThe ability of cells of the human monocyte/macrophage lineage to host HIV-1 replication while resisting cell death is believed to significantly contribute to their ability to serve as a reservoir for viral replication in the host. Although macrophages are generally resistant to apoptosis, interruption of anti-apoptotic pathways can render them susceptible to apoptosis. Here we report that HIV-1(BAL )infection of primary human monocyte-derived macrophages (MDM) upregulates the mRNA and protein levels of the anti-apoptic gene, Bcl-2. Furthermore, this upregulation can be quantitatively mimicked by treating MDM with soluble HIV-1 Tat-86 protein. These results suggest that in infecting cells of the monocyte/macrophage lineage, HIV-1 may be benefiting from additional protection against apoptosis caused by specific upregulation of cellular anti-apoptotic genes.lld:pubmed
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pubmed-article:11914580pubmed:authorpubmed-author:ZhangMingjieMlld:pubmed
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pubmed-article:11914580pubmed:authorpubmed-author:DaytonAndrew...lld:pubmed
pubmed-article:11914580pubmed:copyrightInfoCopyright 2002 National Science Council, ROC and S. Karger AG, Basellld:pubmed
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pubmed-article:11914580pubmed:volume9lld:pubmed
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pubmed-article:11914580pubmed:pagination133-9lld:pubmed
pubmed-article:11914580pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:11914580pubmed:articleTitleBcl-2 upregulation by HIV-1 Tat during infection of primary human macrophages in culture.lld:pubmed
pubmed-article:11914580pubmed:affiliationDivision of Emerging and Transfusion Transmitted Diseases, Office of Blood Research and Review, Center for Biologics Evaluation and Research, Rockville, MD 20852-1448, USA.lld:pubmed
pubmed-article:11914580pubmed:publicationTypeJournal Articlelld:pubmed
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