Peisong Ma, PhD
Assistant Professor, Department of Medicine
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Peisong Ma, PhD
Assistant Professor, Department of Medicine
Research Insterests
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.
Publications
- A regulatory node involving Gαq, PLCβ, and RGS proteins modulates platelet reactivity to critical agonists
- Novel Strategy to Combat the Procoagulant Phenotype in Heparin-Induced Thrombocytopenia Using 12-LOX Inhibition
- GRK2 regulates ADP signaling in platelets via P2Y1 and P2Y12
- Human and mouse PAR4 are functionally distinct receptors: Studies in novel humanized mice
- G protein–coupled receptor kinase 5 regulates thrombin signaling in platelets via PAR-1