GPVI and integrin αIIbβ3 signaling in platelets

Authors

  • S. P. WATSON,

    1. Division of Medical Sciences, Centre for Cardiovascular Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Birmingham, UK
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  • J. M. AUGER,

    1. Division of Medical Sciences, Centre for Cardiovascular Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Birmingham, UK
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  • O. J. T. McCARTY,

    1. Division of Medical Sciences, Centre for Cardiovascular Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Birmingham, UK
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  • A. C. PEARCE

    1. Division of Medical Sciences, Centre for Cardiovascular Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Birmingham, UK
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S. P. Watson, Division of Medical Sciences, Centre for Cardiovascular Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Birmingham B15 2TT, UK.
Tel.: +44 121 4156514; fax: +44 121 4158817; e-mail: s.p.watson@bham.ac.uk

Abstract

Summary.  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 αIIbβ3 (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 γ2. The significance of these signaling cascades in platelet adhesion and platelet aggregation at arterial rates of shear is discussed.

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