Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-9-9
pubmed:abstractText
Genistein, a tyrosine kinase inhibitor, had no or only slight inhibitory effects on platelet aggregation or serotonin release induced by thrombin, while intracellular Ca2+ concentration ([Ca2+]i) elevation was substantially attenuated. It also inhibited the cyclooxygenase pathway, but this effect was not directly related to the suppressive effect of genistein on [Ca2+]i elevation. In order to clarify the mechanism by which genistein suppresses Ca2+ mobilization, its effect was examined on inositol phospholipid metabolism. The production of inositol-1,4,5-trisphosphate was inhibited by genistein in a dose-dependent manner, while 47 kDa protein phosphorylation or phosphatidic acid formation was not affected, suggesting that genistein does not inhibit phospholipase C activity. Pretreatment of unstimulated platelets with genistein increased the amount of phosphatidylinositol-4-monophosphate [PI(4)P], while that of phosphatidylinositol-4,5-bisphosphate [PI(4,5)P2] was reduced. Thrombin stimulation of genistein-pretreated cells intensified this tendency, i.e. a further increase in the amount of PI(4)P and a decrease in the amount of PI(4,5)P2 in an inversely proportional manner. Taken together, these findings imply that genistein acted at the step of PI(4)P 5-kinase which produces PI(4,5)P2 from PI(4)P. Protein tyrosine phosphorylation induced by thrombin was not affected by genistein, suggesting that the inhibitory effect of genistein on polyphosphoinositides was unrelated to tyrosine kinase inhibition.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
3
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
395-403
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Effects of genistein, a tyrosine kinase inhibitor, on platelet functions. Genistein attenuates thrombin-induced Ca2+ mobilization in human platelets by affecting polyphosphoinositide turnover.
pubmed:affiliation
Department of Clinical and Laboratory Medicine, Yamanashi Medical College, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't