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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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INTRODUCTION Introduction References ADHESION IS REQUIRED for cell growth, differentiation, survival, and function. Nowhere is this more evident than in the response to tissue injury, where vascular damage triggers reparative processes, such as hemostasis, inflammation, and wound healing. These processes depend on a coordinated series of cell adhesion and migration events by platelets, leukocytes, and vascular cells for their successful execution.1 Cell adhesion is mediated by a structurally diverse group of plasma membrane receptors, each exhibiting specialized ligand-binding properties that are needed for specific tasks in the injury response. For example, when blood flows through a damaged blood vessel, leukocytes slow down and roll on the endothelial surface as a consequence of the interaction of appropriate sialyl Lewis X-rich membrane glycoproteins on the leukocytes with selectins on the endothelial cells.2,3 Platelets also roll under conditions of high shear on perturbed endothelium4 as well as on denuded vascular surfaces, in the latter case through interactions of the platelet glycoprotein (GP) Ib-V-IX complex with von Willebrand factor (vWF) in the subendothelial matrix.
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Selventa
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