The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/2000/1/139/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 1, January 3, 2000 139-146

Original Article

Regulation of c-Jun NH2-terminal Kinase ( Jnk) Gene Expression during T Cell Activation

Linda Weissa, Alan J. Whitmarshb, Derek D. Yangc, Mercedes Rincóna, Roger J. Davisb, and Richard A. Flavellc

a Immunobiology Program, Department of Medicine, University of Vermont, Burlington, Vermont 05405
b Howard Hughes Medical Institute, Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01605
c Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520
Department of Medicine/Immunobiology Program, Given Medical Bldg. D-305, University of Vermont, Burlington, VT 05405.802-656-3854802-656-0937

mrincon{at}zoo.uvm.edu

The c-Jun NH2-terminal kinases (JNKs) are a group of mitogen-activated protein (MAP) kinases that participate in signal transduction events mediating specific cellular functions. Activation of JNK is regulated by phosphorylation in response to cellular stress and inflammatory cytokines. Here, we demonstrate that JNK is regulated by a second, novel mechanism. Induction of Jnk gene expression is required in specific tissues before activation of this signaling pathway. The in vivo and in vitro ligation of the T cell receptor (TCR) leads to induction of JNK gene and protein expression. TCR signals are sufficient to induce JNK expression, whereas JNK phosphorylation also requires CD28-mediated costimulatory signals. Therefore, both expression and activation contribute to the regulation of the JNK pathway to ensure proper control during the course of an immune response.

Key Words: c-Jun NH2-terminal kinase • gene expression • T cells • phosphorylation • signal transduction

D.D. Yang's present address is Lilly Research Laboratory, Eli Lilly and Co., Indianapolis, IN 46285.

Abbreviations used in this paper: AP-1, activator protein 1; ERK, extracellular signal–regulated kinase; GST, glutathione S-transferase; JNK, c-Jun NH2-terminal kinase; MAP, mitogen-activated protein; MKK, MAP kinase kinase; SAPK, stress-activated protein kinase; SEB, staphylococcal enterotoxin B.

© 2000 The Rockefeller University Press


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