Peisong Ma, PhD

Assistant Professor of Medicine

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Contact

1020 Locust St.
Suite 394
Philadelphia, PA 19107

Email Peisong Ma

215-955-3966
215-955-9170 fax

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Peisong Ma, PhD

Assistant Professor of Medicine

Education

Education

National University of Singapore, Singapore - 2004

Fellowship

University of Pennsylvania

Publications

Dr. Ma’s laboratory is involved with investigations in the areas of thrombosis and hemostasis, with a special emphasis on understanding GPCR (G-protein coupled receptor) and G-protein mediated platelet activation. 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 following is a brief summary of major ongoing projects in the lab.

Project 1: RGS-insensitive Gq (G188S) as probes of G protein Functions

We recently develop a mutant mouse line with a mutation (G188S) in Gq subunit that renders the G protein resistant to interaction with RGS (regulator of G protein signaling) proteins as a class. In contrast to enhanced Gi2 signaling in Gi2(G184S) mutant platelets, we have observed decreased platelet activation in Gq(G188S) mutant mice, suggesting that the negative feedback of Gq regulation is different from that of Gi2. An ongoing study is to fully characterize the effect of G188S mutation on platelet function and thrombus formation.

Project 2: The signaling machinery that provides negative feedback regulation to G protein-dependent signaling during platelet activation

Using CRISPR-Cas9 genome editing, we have recently determined that multiple components of the platelet-signaling network are integrated to mediate GPCRs and G protein-dependent pathways. Ongoing studies are to characterize the mechanisms by which these molecules impact platelet functions, thrombus formation both in vitro and in vivo. To accomplish these goals, we make use of several recently generated mutant mouse lines, intravital microscopy approach and other biochemical techniques.

Project 3: The regulatory networks that regulate platelet activation downstream of G protein signaling using Genome-wide screening

We established that αIIbβ3 activation as readout for genome-wide pooled CRISPR-Cas9 screen in primary megakaryocytes. We will identify novel positive regulators and negative regulators that control integrin activation in response to GPCR-coupled agonists.