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    JNK (c-Jun NH2-terminal kinase) is a target for antioxidants in T lymphocytes.

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    Authors
    Gómez del Arco, Pablo
    Martínez-Martínez, Sara
    Calvo, Victor
    Armesilla, Angel Luis
    Redondo, Juan Miguel
    Issue Date
    1996
    Submitted date
    2007-01-24
    
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    Abstract
    AP-1 has been shown to behave as a redox-sensitive transcription factor that can be activated by both oxidant and antioxidant stimuli. However, the mechanisms involved in the activation of AP-1 by antioxidants are largely unknown. In this study we show that the structurally unrelated antioxidant agents pyrrolidine dithiocarbamate (PDTC), butylated hydroxyanisole, and Nacetylcysteine activated JNK (c-Jun NH2-terminal kinase) in Jurkat T cells. This activation differed substantially from that mediated by phorbol 12-myristate 13-acetate (PMA) and Ca2+ ionophore or produced by costimulation with antibodies against the T cell receptor-CD3 complex and to CD28. The activation of JNK by classical T cell stimuli was transient, whereas that mediated by PDTC and butylated hydroxyanisole (but not N-acetylcysteine) was sustained. The kinetics of JNK activation correlated with the expression of c-jun which was transient after stimulation with PMA plus ionophore and prolonged in response to PDTC, which also transiently induced c-fos. In addition, JNK activation by PMA plus ionophore was sensitive to inhibitors of signaling pathways involving Ca2+, protein kinase C, and tyrosine phosphorylation, which failed to inhibit the activation mediated by PDTC. Transfection of trans-dominant negative expression vectors of ras and raf, together with AP-1-dependent reporter constructs, as well as Western blot analysis using anti-ERK (extracellular signal-regulated kinase) antibodies, indicated that the Ras/Raf/ERK pathway did not appear to mediate the effect of the antioxidant. However, the combined treatment with PDTC and PMA, two agents that synergize on AP-1 activation, resulted in the persistent phosphorylation of ERK-2. In conclusion, our results identify JNK as a target of antioxidant agents which can be regulated differentially under oxidant and antioxidant conditions.
    Citation
    The Journal of Biological Chemistry, 271(42): 26335-26340
    Publisher
    American Society for Biochemistry and Molecular Biology
    URI
    http://hdl.handle.net/2436/7739
    PubMed ID
    8824287
    Additional Links
    http://www.jbc.org/cgi/reprint/271/42/26335
    Type
    Journal article
    Language
    en
    ISSN
    0021-9258
    Collections
    Research Institute in Healthcare Science

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