University of Wolverhampton
Browse
Collection All
bullet
bullet
bullet
bullet
Listed communities
bullet
bullet
bullet
bullet
bullet
bullet
bullet
bullet
bullet
bullet
bullet
bullet
bullet

Wolverhampton Intellectual Repository and E-Theses > Research Institutes > Research Institute in Healthcare Science > Molecular Pharmacology Research Group > JNK (c-Jun NH2-terminal kinase) is a target for antioxidants in T lymphocytes.

Please use this identifier to cite or link to this item: http://hdl.handle.net/2436/7739
    Del.icio.us     LinkedIn     Citeulike     Connotea     Facebook     Stumble it!



Title: JNK (c-Jun NH2-terminal kinase) is a target for antioxidants in T lymphocytes.
Authors: Gómez del Arco, Pablo
Martínez-Martínez, Sara
Calvo, Victor
Armesilla, Angel Luis
Redondo, Juan Miguel
Citation: The Journal of Biological Chemistry, 271(42): 26335-26340
Publisher: American Society for Biochemistry and Molecular Biology
Issue Date: 1996
URI: http://hdl.handle.net/2436/7739
PubMed ID: 8824287
Additional Links: http://www.jbc.org/cgi/reprint/271/42/26335
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.
Type: Article
Language: en
Keywords: JNK
c-Jun NH2-terminal kinase
Antioxidants
T Lymphocytes
ISSN: 0021-9258
Appears in Collections: Molecular Pharmacology Research Group

Files in This Item:
File Description Size Format View/Open
Armesilla6.pdf483KbAdobe PDFThumbnail
View/Open

Related articles on PubMed
bullet
bullet
bullet
bullet
Activation of ERK and JNK1 MAP kinases in cultured lung tissue.
Shapiro P, Absher PM, Posada JP, Evans JN
1997 Aug
bullet
See all 156 articles

All Items in WIRE are protected by copyright, with all rights reserved, unless otherwise indicated.

 

Fairtrade - Guarantees a better deal for Third World Producers

University of Wolverhampton, Wulfruna Street, Wolverhampton, WV1 1LY

Course enquiries: 0800 953 3222, General enquiries: 01902 321000,
Email: enquiries@wlv.ac.uk | Freedom of Information | Disclaimer and copyright | Website feedback | The University as a charity

OR Logo Powered by Open Repository | Cookies