Background Most platelet agonists work through G protein-coupled receptors, activating
pathways that involve members of the G q, G i, and G 12/G 13 families of heterotrimeric G
proteins. G q signaling has been shown to be critical for efficient platelet activation. Growing
evidence suggests that regulatory mechanisms converge on G protein-coupled receptors
and G q to prevent overly robust platelet reactivity. Objectives To identify and characterize
mechanisms by which G q signaling is regulated in platelets. Methods Based on our prior …