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Mammalian platelets are small anucleate blood cells specialized to continuously monitor and preserve the integrity of the cardiovascular system (hemostasis). Platelet plug formation at sites of vascular injury depends on a high sensitivity of platelets towards agonists and a signaling machinery that facilitates a rapid shift from an anti-adhesive to a pro-adhesive state. This high sensitivity poses a risk for premature platelet clearance in circulation (potentially causing thrombocytopenia), and for excessive platelet adhesion and thrombosis at sites of atherosclerotic plaque rupture. Thus, platelet activation needs to be tightly regulated to facilitate hemostasis and to prevent both thrombocytopenia and thrombosis. My lab utilizes transgenic mice and state-of-the-art imaging technologies to investigate the molecular mechanisms regulating platelet activation at sites of vascular injury.