Author(s): Brass LF, Manning DR, Cichowski K, Abrams CS
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Abstract Many of the agonists that cause platelet activation are thought to do so by interacting with G protein-coupled receptors on the platelet surface. By activating heterotrimeric G proteins, these receptors evoke shape change, granule secretion and platelet aggregation. This review provides a brief overview of these events, summarizes current information about the role of pleckstrin in events downstream from G protein-coupled receptors, and briefly considers the signaling pathways that couple G protein activation to the low molecular weight GTP-binding proteins which control cytoskeletal reorganization and fibrinogen receptor exposure during platelet activation.
This article was published in Thromb Haemost
and referenced in Journal of Antivirals & Antiretrovirals