Dr. Ma’s laboratory is involved with investigating thrombosis and hemostasis, with a special emphasis on understanding GPCR (G-protein coupled receptor) and G-protein mediated platelet activation. Many antiplatelet drugs target GPCRs and G protein signaling pathways. Our current studies provide novel insights into the regulatory mechanisms that allow platelets to produce an optimal response to vascular injury. Using well-established vascular injury models, CRISRP-Cas9 genome-editing, and biochemical approaches, we have provided strong evidence that defects in GPCR and G-protein signaling pathways translate into in vivo phenotypes.
The function of GRKs in hemostasis and thrombosis
We have recently provided strong evidence that GPCR kinases (GRKs) are critical negative regulators during platelet activation. Our goals are to investigate how GRKs regulate GPCRs during platelet activation and thrombus formation.
The regulatory networks that regulate platelet activation
Current studies are investigating novel positive regulators and negative regulators in response to GPCR-coupled agonists using genome-wide CRISPR-Cas9 screen.
RGS-insensitive Gq (G188S) as probes of G protein functions
An ongoing study is to characterize the effect of G188S mutation on platelet function and thrombus formation downstream of GPCR-dependent signaling pathways.