Publikationsdatum:
1997-08-01
Beschreibung:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dickens, M -- Rogers, J S -- Cavanagh, J -- Raitano, A -- Xia, Z -- Halpern, J R -- Greenberg, M E -- Sawyers, C L -- Davis, R J -- CA43855/CA/NCI NIH HHS/ -- CA65861/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Aug 1;277(5326):693-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉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.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9235893" target="_blank"〉PubMed〈/a〉
Schlagwort(e):
Activating Transcription Factor 2
;
Animals
;
COS Cells
;
Calcium-Calmodulin-Dependent Protein Kinases/*metabolism
;
Carrier Proteins/chemistry/*metabolism
;
Cell Nucleus/metabolism
;
Cell Transformation, Neoplastic
;
Cells, Cultured
;
Cloning, Molecular
;
Cyclic AMP Response Element-Binding Protein/metabolism
;
Cytoplasm/metabolism
;
Fusion Proteins, bcr-abl/metabolism
;
Gene Expression Regulation
;
JNK Mitogen-Activated Protein Kinases
;
Mitogen-Activated Protein Kinase 9
;
*Mitogen-Activated Protein Kinases
;
Molecular Sequence Data
;
Phosphorylation
;
Protein Kinases/metabolism
;
Proto-Oncogene Proteins c-jun/metabolism
;
Recombinant Fusion Proteins/metabolism
;
*Signal Transduction
;
Transcription Factors/metabolism
;
Transcriptional Activation
;
Transfection
Print ISSN:
0036-8075
Digitale ISSN:
1095-9203
Thema:
Biologie
,
Chemie und Pharmazie
,
Informatik
,
Medizin
,
Allgemeine Naturwissenschaft
,
Physik
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