Work

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

Year: 2000

Type: article

Abstract: The c-Jun NH(2)-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.

Source: The Journal of Experimental Medicine

DOI: 10.1084/jem.191.1.139

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

Institutions: University of Vermont, Howard Hughes Medical Institute, University of Massachusetts Chan Medical School, Yale University

Language: English

Topic: Protein Kinase Regulation and GTPase Signaling

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: green

Funders: National Institutes of Health, National Cancer Institute, National Institute of Allergy and Infectious Diseases