Source:http://linkedlifedata.com/resource/pubmed/id/15093750
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2004-4-19
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| pubmed:abstractText |
Patients infected with human immunodeficiency virus type 1 (HIV-1) develop a spectrum of B cell lymphoproliferative disorders ranging from polyclonal B cell activation to B cell lymphomas. While a direct role of Epstein-Barr virus (EBV) is well recognized for most of these lesions, recent findings have suggested that transactivator HIV-1 Tat protein might be involved in the pathogenesis of B cell lymphomas. Tat-expressing EBV-positive B cells were generated by transduction with a retroviral Tat-encoding vector. B(Tat+) cells expressed lower levels of anti-apoptotic protein Bcl-2 than parental and control B(Tat-) cells, generated by transduction with an empty retroviral vector, and were more prone to apoptosis upon serum withdrawal, as assessed by analysis of annexin V-stained cells and cleavage of poly-ADP-ribose-polymerase by caspase 3. Nevertheless, in serum starvation, B(Tat-) cells mainly exhibited the Rb hypo-phosphorylated form, underwent cell cycle arrest, and grew in single cell suspension, while B(Tat+) cells displayed the Rb hyper-phoshorylated form, progressed throughout the cell cycle, and retained the ability to grow in small clumps. Finding that B(Tat+) cells maintained proliferative capacity upon serum withdrawal suggests that cells expressing Tat have growth advantages among the EBV-driven cell proliferations and may originate B cell clones with more oncogenic potential.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Annexin A5,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Serum-Free,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, tat,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/tat Gene Products, Human...
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
0014-4827
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
295
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
539-48
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:15093750-Annexin A5,
pubmed-meshheading:15093750-Apoptosis,
pubmed-meshheading:15093750-B-Lymphocytes,
pubmed-meshheading:15093750-Caspases,
pubmed-meshheading:15093750-Cell Cycle,
pubmed-meshheading:15093750-Cell Division,
pubmed-meshheading:15093750-Cell Line,
pubmed-meshheading:15093750-Cell Line, Transformed,
pubmed-meshheading:15093750-Cell Transformation, Viral,
pubmed-meshheading:15093750-Culture Media, Serum-Free,
pubmed-meshheading:15093750-Gene Expression Regulation, Viral,
pubmed-meshheading:15093750-Gene Products, tat,
pubmed-meshheading:15093750-HIV-1,
pubmed-meshheading:15093750-Herpesvirus 4, Human,
pubmed-meshheading:15093750-Humans,
pubmed-meshheading:15093750-Phosphorylation,
pubmed-meshheading:15093750-Retinoblastoma,
pubmed-meshheading:15093750-Retroviridae,
pubmed-meshheading:15093750-Viral Proteins,
pubmed-meshheading:15093750-tat Gene Products, Human Immunodeficiency Virus
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| pubmed:year |
2004
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| pubmed:articleTitle |
Human immunodeficiency virus type 1 Tat protein modulates cell cycle and apoptosis in Epstein-Barr virus-immortalized B cells.
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| pubmed:affiliation |
Department of Oncology and Surgical Sciences, Section of Oncology, University of Padova, Padua, Italy.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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