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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5326
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pubmed:dateCreated |
1997-8-14
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pubmed:databankReference |
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pubmed:abstractText |
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.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Activating Transcription Factor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Calmodulin-Dependent...,
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/JNK Mitogen-Activated Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 9,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-jun,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0036-8075
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
277
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
693-6
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:9235893-Activating Transcription Factor 2,
pubmed-meshheading:9235893-Animals,
pubmed-meshheading:9235893-COS Cells,
pubmed-meshheading:9235893-Calcium-Calmodulin-Dependent Protein Kinases,
pubmed-meshheading:9235893-Carrier Proteins,
pubmed-meshheading:9235893-Cell Nucleus,
pubmed-meshheading:9235893-Cell Transformation, Neoplastic,
pubmed-meshheading:9235893-Cells, Cultured,
pubmed-meshheading:9235893-Cloning, Molecular,
pubmed-meshheading:9235893-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:9235893-Cytoplasm,
pubmed-meshheading:9235893-Fusion Proteins, bcr-abl,
pubmed-meshheading:9235893-Gene Expression Regulation,
pubmed-meshheading:9235893-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:9235893-Mitogen-Activated Protein Kinase 9,
pubmed-meshheading:9235893-Mitogen-Activated Protein Kinases,
pubmed-meshheading:9235893-Molecular Sequence Data,
pubmed-meshheading:9235893-Phosphorylation,
pubmed-meshheading:9235893-Protein Kinases,
pubmed-meshheading:9235893-Proto-Oncogene Proteins c-jun,
pubmed-meshheading:9235893-Recombinant Fusion Proteins,
pubmed-meshheading:9235893-Signal Transduction,
pubmed-meshheading:9235893-Transcription Factors,
pubmed-meshheading:9235893-Transcriptional Activation,
pubmed-meshheading:9235893-Transfection
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pubmed:year |
1997
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pubmed:articleTitle |
A cytoplasmic inhibitor of the JNK signal transduction pathway.
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pubmed:affiliation |
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.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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