Adhesion of human and mouse platelets to collagen under shear: a unifying model Jocelyn M. Auger * ,† ,1 , Marijke J. E. Kuijpers † , Yotis A. Senis * , Steve P. Watson * and Johan W. M. Heemskerk † * Centre for Cardiovascular Sciences, Division of Medical Sciences, Institute of Biomedical Research, The Medical School, University of Birmingham, Edgbaston, Birmingham, UK; and † Department of Biochemistry, Cardiovascular Research Institute Maastricht, University of Maastricht, Maastricht, The Netherlands 1 Correspondence: Centre for Cardiovascular Sciences, Division of Medical Sciences, Institute of Biomedical Research, Wolfson Dr., The Medical School, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. E-mail: jma299@bham.ac.uk; jwm.heemskerk@bioch.unimass.hl <h3>SPECIFIC AIMS</h3> Our understanding of the mechanisms that underlie platelet adhesion and thrombus formation under arterial shear conditions have altered significantly over the past 25 years. Key roles for the leucine-rich von Willebrand factor (VWF) receptor glycoprotein (GP) Ib-IX-V and the integrin αIIbß3 in platelet tethering and aggregate formation are established. However, the precise interplay of the collagen receptors, the immunoglobulin GPVI and the integrin α2ß1, in supporting adhesion and aggregate formation on collagen is unclear. Differences between human and mouse have been proposed. Src kinases play a central role
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