| Literature DB >> 9235893 |
M Dickens1, J S Rogers, J Cavanagh, A Raitano, Z Xia, J R Halpern, M E Greenberg, C L Sawyers, R J Davis.
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.Entities:
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Year: 1997 PMID： 9235893 DOI： 10.1126/science.277.5326.693
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728