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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 2
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pubmed:dateCreated |
1994-3-9
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pubmed:abstractText |
We examined the effect of various tyrosine kinase inhibitors on basic fibroblast growth factor (bFGF)-induced cell signaling and DNA synthesis in coronary venular endothelial cells (CVEC). Two tyrosine kinase inhibitors, genistein and methyl 2,5-dihydroxycinnamate, showed reversible, dose-dependent inhibition of bFGF-stimulated DNA synthesis in CVEC with half-maximal inhibitory concentrations of 12 and 3 microM, respectively. Both compounds exhibited preferential inhibition of bFGF vs. serum-induced DNA synthesis. bFGF stimulated increased tyrosine phosphorylation of CVEC cellular proteins, including the FGF receptor, which were visible within 1 min of treatment. Concomitant with their effect on DNA synthesis, both compounds exhibited dose-dependent inhibition of tyrosine phosphorylation of intracellular substrates induced by bFGF. A 2-h pretreatment of quiescent CVEC with genistein blocked nuclear translocation but not cytoplasmic internalization of bFGF, whereas the same treatment with methyl 2,5-dihydroxycinnamate inhibited both processes. These results suggest that activation of bFGF receptor tyrosine kinase activity plays a role in nuclear translocation of bFGF and initiation of DNA synthesis in endothelial cells.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cinnamates,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Fibroblast Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Genistein,
http://linkedlifedata.com/resource/pubmed/chemical/Isoflavones,
http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine,
http://linkedlifedata.com/resource/pubmed/chemical/methyl 2,5-dihydroxycinnamate
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
266
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H107-20
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:8304491-Animals,
pubmed-meshheading:8304491-Cattle,
pubmed-meshheading:8304491-Cell Line,
pubmed-meshheading:8304491-Cell Nucleus,
pubmed-meshheading:8304491-Cinnamates,
pubmed-meshheading:8304491-Coronary Vessels,
pubmed-meshheading:8304491-DNA,
pubmed-meshheading:8304491-Dose-Response Relationship, Drug,
pubmed-meshheading:8304491-Endothelium, Vascular,
pubmed-meshheading:8304491-Fibroblast Growth Factors,
pubmed-meshheading:8304491-Genistein,
pubmed-meshheading:8304491-Isoflavones,
pubmed-meshheading:8304491-Kinetics,
pubmed-meshheading:8304491-Phosphorylation,
pubmed-meshheading:8304491-Protein-Tyrosine Kinases,
pubmed-meshheading:8304491-Signal Transduction,
pubmed-meshheading:8304491-Tyrosine
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pubmed:year |
1994
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pubmed:articleTitle |
Tyrosine kinase inhibitors impair fibroblast growth factor signaling in coronary endothelial cells.
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pubmed:affiliation |
Microcirculation Research Institute, College of Medicine, Texas A & M University Health Science Center, College Station 77843.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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