Abstract

This review summarizes recent developments in our understanding of the molecular basis of platelet activation by two distinct types of surface receptor, the immunoglobulin GPVI, and the integrin alphaIIb beta3 (also known as GPIIbIIIa). These two classes of receptor signal through similar yet distinct tyrosine kinase-based signaling cascades leading to activation of phospholipase C gamma2. The significance of these signaling cascades in platelet adhesion and platelet aggregation at arterial rates of shear is discussed.

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