A model for modulating platelet reactivity through regulated control of RGS proteins. Platelets can achieve free RGS18 levels by ≥3 states: resting (inactive), after activation by agonist (active; thrombin stimulation), and resistance to activation (active; PGI2-mediated suppression). AC, adenylyl cyclase; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; DAG, diacylglycerol; GTP, guanosine triphosphate; IP, prostacyclin; PIP, phosphatidylinositol 4,5-bisphosphate; PKA, protein kinase A; PLC, phospholipase C; SFK, Src family kinases; TxA2, thromboxane A2. See Figure 7 in the article by Ma et al that begins on page 2611.
