Hemostasis is the physiologic process that stops bleeding following a breach in the vasculature. Disruption of various components of the hemostatic system can have disastrous consequences for humans, including excessive bleeding or hemorrhage when hemostasis is insufficient (e.g. hemophilia, thrombocytopenia, etc), or thrombosis when the hemostatic machinery is activated inappropriately (e.g. myocardial infarction, stroke, DVT/PE). The goal of our research is to gain a better understanding of the mechanisms that regulate hemostasis and thrombosis in vivo. In particular, we are interested in how multiple signaling inputs present at a site of vascular injury are integrated to regulate the cellular and biochemical effectors of the hemostatic system. The following is a brief summary of major ongoing projects.