Signaling through G proteins in platelets: to the integrins and beyond.
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.
Brass
L F
LF
Department of Medicine, University of Pennsylvania, Philadelphia 19104, USA. brass@mail.med.upenn.edu
Manning
D R
DR
Cichowski
K
K
Abrams
C S
CS
D001798:Blood Proteins / Q000502:physiology; D004837:Epinephrine / Q000097:blood; D019204:GTP-Binding Proteins / Q000097:blood / Q000502:physiology*; D006801:Humans; D016023:Integrins / Q000502:physiology*; D008970:Molecular Weight; D010750:Phosphoproteins; D015539:Platelet Activation; D015398:Signal Transduction / Q000502:physiology*; D013928:Thromboxane A2 / Q000097:blood
D001798:Blood Proteins; D016023:Integrins; D010750:Phosphoproteins; C039077:platelet protein P47; D013928:Thromboxane A2; D019204:GTP-Binding Proteins; D004837:Epinephrine