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rdf:type |
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lifeskim:mentions |
umls-concept:C0033684,
umls-concept:C0034678,
umls-concept:C0037083,
umls-concept:C1332768,
umls-concept:C1364684,
umls-concept:C1413549,
umls-concept:C1514873,
umls-concept:C1546857,
umls-concept:C1556066,
umls-concept:C1619636,
umls-concept:C1704803,
umls-concept:C1704804,
umls-concept:C1710082
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pubmed:issue |
3
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pubmed:dateCreated |
1998-12-7
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pubmed:databankReference |
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pubmed:abstractText |
Kinase suppressor of ras (ksr) is required for efficient signal transmission within the RAS/MAPK cascade. A screen for mutations that modify a ksr-dependent phenotype identified a novel gene, connector enhancer of ksr (cnk), that functions upstream or in parallel to RAF in the RAS pathway. cnk encodes a protein containing several protein-protein interaction domains, suggesting that it brings different signaling molecules together. CNK is required in multiple receptor tyrosine kinase pathways where it appears to be a tyrosine phosphorylation target. Finally, CNK physically interacts with RAF and appears to localize to cell-cell contact regions. Together, these findings suggest that CNK is a novel component of a RAS-dependent signaling pathway that regulates RAF function and/or targets RAF to a specific subcellular compartment upon RAS activation.
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0092-8674
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pubmed:author |
|
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pubmed:issnType |
Print
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pubmed:day |
30
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pubmed:volume |
95
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
343-53
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:9814705-Adaptor Proteins, Signal Transducing,
pubmed-meshheading:9814705-Amino Acid Sequence,
pubmed-meshheading:9814705-Animals,
pubmed-meshheading:9814705-Carrier Proteins,
pubmed-meshheading:9814705-Cell Differentiation,
pubmed-meshheading:9814705-Cell Line,
pubmed-meshheading:9814705-Cell Survival,
pubmed-meshheading:9814705-Drosophila Proteins,
pubmed-meshheading:9814705-Drosophila melanogaster,
pubmed-meshheading:9814705-Evolution, Molecular,
pubmed-meshheading:9814705-Eye,
pubmed-meshheading:9814705-Genes, Dominant,
pubmed-meshheading:9814705-Genes, Suppressor,
pubmed-meshheading:9814705-Humans,
pubmed-meshheading:9814705-Insect Proteins,
pubmed-meshheading:9814705-Intercellular Junctions,
pubmed-meshheading:9814705-Molecular Sequence Data,
pubmed-meshheading:9814705-Mutagenesis,
pubmed-meshheading:9814705-Phenotype,
pubmed-meshheading:9814705-Phosphorylation,
pubmed-meshheading:9814705-Protein Kinases,
pubmed-meshheading:9814705-Proto-Oncogene Proteins c-raf,
pubmed-meshheading:9814705-Receptor Protein-Tyrosine Kinases,
pubmed-meshheading:9814705-Signal Transduction,
pubmed-meshheading:9814705-Wing,
pubmed-meshheading:9814705-ras Proteins
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pubmed:year |
1998
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pubmed:articleTitle |
CNK, a RAF-binding multidomain protein required for RAS signaling.
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pubmed:affiliation |
Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley 94720-3200, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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