My research has progressed from a general interest in molecular signaling pathways that regulate important biological events such as cell adhesion to a more focused analysis of signaling pathways that regulate human platelet and megakaryocyte activation during normal blood clotting (hemostasis) or pathological aggregate formation (thrombosis). Precise control of platelet function is crucial for vascular health since excessive activation can lead to ischemic events such as myocardial infarction and stroke, which are still the primary causes of death in the United States. While current anti-platelet drugs are effective, they cause clinically significant bleeding and do not prevent thrombosis in all patient populations, which highlights a need for safer therapeutics that benefit more high-risk groups.
One of my immediate goals has been to identify novel signaling molecules that positively regulate integrin adhesion receptors on human platelets. In collaboration with others, we discovered an enzyme known as arylacetamide deacetylase-like 1 (AADACL1) in platelets and megakaryocytes using a combination of library screening and innovative chemoproteomic profiling. We demonstrated that AADACL1 regulates important signal transduction pathways during platelet activation and thrombus formation. I am currently evaluating physiological role(s) of AADACL1 in rat models of thrombosis and hemostasis.