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Redox events in HTLV-1 tax-induced apoptotic T-cell death
(Division of Cellular Immunology (G0100), Tumor Immunology Program, German Cancer Research Center, Im Neuenheimer Feld 280, D69120 Heidelberg, Germany)
Department of Immunology and Cell Biology, University of Muenster, Roentgenstr. 21, D-48149 Muenster, Germany.ORCID iD: 0000-0001-9518-1411
Department of Immunology and Cell Biology, University of Muenster, Roentgenstr. 21, D-48149 Muenster, Germany.
INSERM U412, Ecole Normale S périeure de Lyon, 69367 Lyon, Cedex 07, France.
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2002 (English)In: Antioxidants and Redox Signaling, ISSN 1523-0864, E-ISSN 1557-7716, Vol. 4, no 3, 471-477 p.Article in journal (Refereed) Published
Abstract [en]

A number of studies implicate reactive oxygen intermediates in the induction of DNA damage and apoptosis. Recent studies suggest that the human T-cell leukemia virus type I (HTLV-1) Tax protein induces oxidative stress and apoptotic T-cell death. Activation of the T-cell receptor/CD3 pathway enhances the Tax-mediated oxidative and apoptotic effects. Tax-mediated apoptosis and oxidative stress as well as activation of nuclear factor-kappaB can be potently suppressed by antioxidants. This review focuses on Tax-dependent changes in the intracellular redox status and their role in Tax-mediated DNA damage and apoptosis. The relevance of these observations to HTLV-1 virus-mediated T-cell transformation and leukemogenesis are discussed.

Place, publisher, year, edition, pages
Mary Ann Liebert, Inc. publishers , 2002. Vol. 4, no 3, 471-477 p.
Keyword [en]
dna-repair, gene-expression, human thioredoxin, leukemia-virus, nf-kappa-b, oxidative stress, prooxidant state, Signaling pathway, transcription factors, virus type-i
National Category
Biochemistry and Molecular Biology Cell Biology
Identifiers
URN: urn:nbn:se:liu:diva-87010DOI: 10.1089/15230860260196263ISI: 000176633600012PubMedID: 12215214OAI: oai:DiVA.org:liu-87010DiVA: diva2:584228
Available from: 2013-01-08 Created: 2013-01-08 Last updated: 2017-12-06

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