Effects of cAMP-Dependent, Calmodulin-Dependent, and C-Type Protein Kinases on Platelet Calcium Transport
Cyclic AMP (cAMP) and Ca2+ are interrelated intracellular messengers known to modify cellular function through specific protein kinases (Cohen, 1982). In platelets, increases in cAMP inhibit platelet activation, an effect that is reversed by inhibitors of adenylate cyclase (Salzman, 1972; Chianget al., 1975), while Ca2+ is involved in activation rather than inhibition of platelet function (Detwileret al., 1978). In addition to cAMP-and calmodulindependent protein kinases, a third kinase is intimately involved in platelet activation—protein kinase C (Kishimotoet al., 1980). This kinase is activated by diacylglycerol, a product of phospholipase C—mediated hydrolysis of phosphatidylinositol.
KeywordsATPase Activity Human Platelet Dependent Protein Kinase Platelet Membrane Internal Membrane
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- Detwiler, T. C., Charo, I. F., and Feinman, R. D., 1978, Evidence that calcium regulates platelet function, Thrombos. Haemostas. 40:207–212.Google Scholar
- Le Peuch, C. J., Le Peuch, D. A. M., Katz, S., DeMaille, J., Hinkle, M. T., Bredoux, R., Enouf, J., Levy-Toledano, S., and Caen, J., 1983, Regulation of calcium accumulation and efflux from platelet membrane vesicles: possible role for cAMP-dependent phosphorylation and calmodulin, Biochim. Biophys. Acta 731:456–464.PubMedCrossRefGoogle Scholar