Regulation of c-Jun NH2-terminal kinase (Jnk) gene expression during T cell activation

Linda Weiss, Alan J. Whitmarsh, Derek D. Yang, Mercedes Rincón, Roger J. Davis, Richard A. Flavell

    Research output: Contribution to journalArticlepeer-review

    Abstract

    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.
    Original languageEnglish
    Pages (from-to)139-145
    Number of pages6
    JournalJournal of Experimental Medicine
    Volume191
    Issue number1
    DOIs
    Publication statusPublished - 3 Jan 2000

    Keywords

    • C-Jun NH2-terminal kinase
    • Gene expression
    • Phosphorylation
    • Signal transduction
    • T cells

    Fingerprint

    Dive into the research topics of 'Regulation of c-Jun NH2-terminal kinase (Jnk) gene expression during T cell activation'. Together they form a unique fingerprint.

    Cite this