Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-10-6
pubmed:abstractText
We have shown that an estradiol-dependent activation of human T cell leukemia virus-I Tax leads to the inhibition of cell proliferation and to the induction of apoptosis. The present study demonstrates that a hormone-dependent activation of Tax promotes an enhanced prooxidant state in stably transfected Jurkat cells as measured by changes in the intracellular levels of glutathione and H2O2; these changes are followed by apoptotic cell death. Additional stimulation of the CD3/TCR pathway enhances the oxidative and apoptotic effects. Both Tax-mediated apoptosis and oxidative stress can be potently suppressed by antioxidants, as is seen with the administration of recombinant thioredoxin (adult T cell leukemia-derived factor) or pyrrolidine dithiocarbamate. Hormone-induced Tax activation induces a long-lasting activation of NF-kappaB, which is a major target of reactive oxygen intermediates. The long-term exposure of Jurkat cells to hormone eventually results in a selection of cell clones that have lost Tax activity. A subsequent transfection of these apparently "nonresponsive" clones allows the recovery of Tax responses in these cells. Our observations indicate that changes in the intracellular redox status may be a determining factor in Tax-mediated DNA damage, apoptosis, and selection against the long-term expression of Tax function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
161
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3050-5
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9743370-Antibodies, Monoclonal, pubmed-meshheading:9743370-Antigens, CD3, pubmed-meshheading:9743370-Antioxidants, pubmed-meshheading:9743370-Apoptosis, pubmed-meshheading:9743370-Drug Synergism, pubmed-meshheading:9743370-Estradiol, pubmed-meshheading:9743370-Gene Products, tax, pubmed-meshheading:9743370-Human T-lymphotropic virus 1, pubmed-meshheading:9743370-Humans, pubmed-meshheading:9743370-Intracellular Fluid, pubmed-meshheading:9743370-Jurkat Cells, pubmed-meshheading:9743370-Lymphocyte Activation, pubmed-meshheading:9743370-Oxidants, pubmed-meshheading:9743370-Oxidation-Reduction, pubmed-meshheading:9743370-Receptor-CD3 Complex, Antigen, T-Cell, pubmed-meshheading:9743370-Receptors, Estrogen, pubmed-meshheading:9743370-Recombinant Fusion Proteins, pubmed-meshheading:9743370-T-Lymphocytes, pubmed-meshheading:9743370-Time Factors, pubmed-meshheading:9743370-Transfection
pubmed:year
1998
pubmed:articleTitle
Human T cell leukemia virus-I (HTLV-I) Tax-mediated apoptosis in activated T cells requires an enhanced intracellular prooxidant state.
pubmed:affiliation
Department of Internal Medicine I, Eberhard-Karls University, Tübingen, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't