A Cytoplasmic Inhibitor of the JNK Signal Transduction Pathway-Reference-Cited by-同舟云学术

A Cytoplasmic Inhibitor of the JNK Signal Transduction Pathway

Published:1997-08 Issue:5326 Volume:277 Page:693-696
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Dickens Martin¹²³,Rogers Jeffrey S.¹²³,Cavanagh Julie¹²³,Raitano Art¹²³,Xia Zhengui¹²³,Halpern Jocelyn R.¹²³,Greenberg Michael E.¹²³,Sawyers Charles L.¹²³,Davis Roger J.¹²³

Affiliation:

1. M. Dickens, J. S. Rogers, J. Cavanagh, R. J. Davis, Howard Hughes Medical Institute and Program in Molecular Medicine, Department of Biochemistry and Molecular Biology, University of Massachusetts Medical School, 373 Plantation Street, Worcester, MA 01605, USA.

2. A. Raitano, J. R. Halpern, C. L. Sawyers, Department of Medicine, University of California School of Medicine, Los Angeles, CA 90095, USA.

3. Z. Xia and M. E. Greenberg, Division of Neuroscience, Department of Neurology, Children's Hospital, and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.

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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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