GSBS Student Publications

Title

A cytoplasmic inhibitor of the JNK signal transduction pathway

GSBS Program

Biochemistry & Molecular Pharmacology

Publication Date

1997-08-01

UMMS Affiliation

Graduate School of Biomedical Sciences; Howard Hughes Medical Institute and Program in Molecular Medicine

Document Type

Article

Disciplines

Life Sciences | Medicine and Health Sciences

Abstract

The c-Jun amino-terminal kinase (JNK) is a member of the stress-activated group of mitogen-activated protein (MAP) kinases that are implicated in the control of cell growth. A murine cytoplasmic protein that binds specifically to JNK [the JNK interacting protein-1 (JIP-1)] was characterized and cloned. JIP-1 caused cytoplasmic retention of JNK and inhibition of JNK-regulated gene expression. In addition, JIP-1 suppressed the effects of the JNK signaling pathway on cellular proliferation, including transformation by the Bcr-Abl oncogene. This analysis identifies JIP-1 as a specific inhibitor of the JNK signal transduction pathway and establishes protein targeting as a mechanism that regulates signaling by stress-activated MAP kinases.

Source

Science. 1997 Aug 1;277(5326):693-6.

Journal/Book/Conference Title

Science (New York, N.Y.)

Related Resources

Link to article in PubMed

PubMed ID

9235893

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