Title
A cytoplasmic inhibitor of the JNK signal transduction pathway
UMMS Affiliation
Graduate School of Biomedical Sciences; Howard Hughes Medical Institute and Program in Molecular Medicine
Publication Date
1997-08-01
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.
DOI of Published Version
10.1126/science.277.5326.693
Source
Science. 1997 Aug 1;277(5326):693-6.
Journal/Book/Conference Title
Science (New York, N.Y.)
Related Resources
PubMed ID
9235893
Repository Citation
Dickens M, Rogers JS, Cavanagh J, Raitano A, Xia Z, Halpern JR, Greenberg ME, Sawyers CL, Davis RJ. (1997). A cytoplasmic inhibitor of the JNK signal transduction pathway. GSBS Student Publications. https://doi.org/10.1126/science.277.5326.693. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/308