rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2006-6-7
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pubmed:abstractText |
The human RIN1 gene was first identified as a cDNA fragment that interfered with RAS-induced phenotypes in the yeast Saccharomyces cerevisiae. Subsequent analysis of full-length RIN1 clones showed that the protein product of this gene is a downstream effector of RAS and binds with high affinity and specificity to activated HRAS. Two downstream RIN1 effector pathways have been described. The first involves direct activation of RAB5-mediated endocytosis. The second involves direct activation of ABL tyrosine kinase activity. Importantly, each of these distinct RIN1 functions is enhanced by activated RAS, suggesting that RIN1 represents a unique class of RAS effector connected to two independent signaling pathways. In this chapter, we summarize our assays and approaches for evaluating the biochemistry and biology of RIN1.
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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 |
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pubmed:status |
MEDLINE
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pubmed:issn |
0076-6879
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
407
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
335-44
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:16757336-Animals,
pubmed-meshheading:16757336-Endocytosis,
pubmed-meshheading:16757336-Evolution, Molecular,
pubmed-meshheading:16757336-Guanosine Diphosphate,
pubmed-meshheading:16757336-Guanosine Triphosphate,
pubmed-meshheading:16757336-Humans,
pubmed-meshheading:16757336-Intracellular Signaling Peptides and Proteins,
pubmed-meshheading:16757336-Proto-Oncogene Proteins c-abl,
pubmed-meshheading:16757336-Proto-Oncogene Proteins p21(ras),
pubmed-meshheading:16757336-rab5 GTP-Binding Proteins
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pubmed:year |
2006
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pubmed:articleTitle |
The RIN family of Ras effectors.
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pubmed:affiliation |
Department of Biological Chemistry, University of California Los Angeles School of Medicine, Los Angeles, California, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, N.I.H., Extramural
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