A cytoplasmic inhibitor of the JNK signal transduction pathway

被引：623

作者：

Dickens, M

Rogers, JS

Cavanagh, J

Raitano, A

Xia, ZG

Halpern, JR

Greenberg, ME

Sawyers, CL

Davis, RJ

机构：

[1] UNIV MASSACHUSETTS, SCH MED, HOWARD HUGHES MED INST, WORCESTER, MA 01605 USA

[2] UNIV MASSACHUSETTS, SCH MED, DEPT BIOCHEM & MOL BIOL, PROGRAM MOL MED, WORCESTER, MA 01605 USA

[3] UNIV CALIF LOS ANGELES, SCH MED, DEPT MED, LOS ANGELES, CA 90095 USA

[4] CHILDRENS HOSP, DEPT NEUROL, DIV NEUROSCI, BOSTON, MA 02115 USA

[5] HARVARD UNIV, SCH MED, DEPT NEUROBIOL, BOSTON, MA 02115 USA

来源：

SCIENCE | 1997年 / 277卷 / 5326期

关键词：

D O I：

10.1126/science.277.5326.693

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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.

引用

页码：693 / 696

页数：4

共 37 条

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