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Blood, 15 June 2007, Vol. 109, No. 12, pp. 5087-5095. Prepublished online as a Blood First Edition Paper on February 20, 2007; DOI 10.1182/blood-2006-12-027698. This Article Full Text (PDF) All Versions of this Article: blood-2006-12-027698v1 109/12/5087    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jackson, S. P Search for Related Content PubMed PubMed Citation Articles by Jackson, S. P Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted December 27, 2006 Accepted February 9, 2007 The growing complexity of platelet aggregation Shaun P Jackson* Australian Centre for Blood Diseases, Monash University, Melbourne, Australia * Corresponding author; email: shaun.jackson{at}med.monash.edu.au. Platelet aggregation, the process by which platelets adhere to other platelets at sites of vascular injury, has long been recognized to be critical for hemostatic plug formation and thrombosis. Until relatively recently, platelet aggregation was considered a straightforward process, involving the non-covalent bridging of integrin IIb3 receptors (GPIIb-IIIa) on the platelet surface by the dimeric adhesive protein fibrinogen. However, with recent technical advances enabling real-time analysis of platelet aggregation in vivo, it has become apparent that this process is much more complex and dynamic than previously anticipated. Over the last decade it has become clear that platelet aggregation represents a multi-step adhesion process involving distinct receptors and adhesive ligands, with the contribution of individual receptor-ligand interactions to the aggregation process dependent on the prevailing blood flow conditions. It now appears that at least 3 distinct mechanisms can initiate platelet aggregation, with each of these mechanisms operating over a specific shear range in vivo. The identification of specific shear-dependent mechanisms of platelet aggregation has raised the possibility that vascular-bed specific inhibitors of platelet aggregation may be developed in the future that are safer and more effective than existing antiplatelet agents. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Gilio, I. C. A. Munnix, P. Mangin, J. M. E. M. Cosemans, M. A. H. Feijge, P. E. J. van der Meijden, S. Olieslagers, M. B. Chrzanowska-Wodnicka, R. Lillian, S. Schoenwaelder, et al. Non-redundant Roles of Phosphoinositide 3-Kinase Isoforms {alpha} and {beta} in Glycoprotein VI-induced Platelet Signaling and Thrombus Formation J. Biol. Chem., December 4, 2009; 284(49): 33750 - 33762. [Abstract] [Full Text] [PDF] B. M. Steele, M. T. Harper, I. C. Macaulay, C. N. Morrell, A. Perez-Tamayo, M. Foy, R. Habas, A. W. Poole, D. J. Fitzgerald, and P. B. Maguire Canonical Wnt signaling negatively regulates platelet function PNAS, November 24, 2009; 106(47): 19836 - 19841. [Abstract] [Full Text] [PDF] O. Neumuller, M. Hoffmeister, J. Babica, C. Prelle, K. Gegenbauer, and A. P. Smolenski Synaptotagmin-like protein 1 interacts with the GTPase-activating protein Rap1GAP2 and regulates dense granule secretion in platelets Blood, August 13, 2009; 114(7): 1396 - 1404. [Abstract] [Full Text] [PDF] F. Banno, A. K. Chauhan, K. Kokame, J. Yang, S. Miyata, D. D. Wagner, and T. 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