Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10721 (c-kit)
 6,575 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously demonstrated PLD activation via c-kit receptor activation in rat peritoneal mast cells (Koike et al. 1993, J. Immunol. 151,359-366). In this study, the mechanism of arachidonic acid (AA) release in stem cell factor (SCF) stimulation was investigated. Genistein, a protein tyrosine kinase inhibitor, was found to inhibit the AA release in SCF-stimulated cells, whereas pretreatment with vanadate, a protein tyrosine phosphatase inhibitor, enhanced the AA release. Propranolol, an inhibitor of phosphatidate (PA) phosphohydrolase, repressed both AA liberation and 1,2-diacylglycerol (1,2-DG) formation. Short pretreatment with phorbol myristate acetate blunted the SCF-induced AA liberation. These results indicate that 1,2-DG generated via the phospholipase D pathway activated by tyrosine phosphorylation is a principle source for AA released in response to SCF in mast cells.
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PMID:SCF/c-kit receptor-mediated arachidonic acid liberation in rat mast cells. Involvement of PLD activation associated tyrosine phosphorylation. 750 46