Postdoctoral Scholar
Division of Research

As for any biological process, vascular permeability can be modulated by a variety of agents utilizing a combination of several signal transduction pathways. My research interests include the study of the activation and the termination of these signaling responses leading to endothelial permeability. I look at the cross talk and the regulation of different Receptor Tyrosine Kinase (RTK) & G-Protein Coupled Receptor (GPCR) mediated (specifically VEGFR2 vs Histamine receptor) signal transduction pathways and their relative role in defining the overall physiological response. In addition, I look at the roles of different beta arrestin isoforms in mediating this cross talk. My other interests include the study of signaling pathways whereby one signal (say, VEGFR activation) can activate more than one opposing physiological responses (angiogenesis vs endothelial permeability response) in the same system. Eventually I plan to integrate these in vitro signal transduction studies into an in vivo model to be able to mimic and modulate the natural physiological changes of disease and injury.

Kumar P, Lau CS, Mathur M, Wang P, DeFea KA. Differential effects of beta-arrestins on the internalization, desensitization and ERK1/2 activation downstream of protease-activated-receptor-2. Am J Physiol Cell Physiol. 2007 Jul; 293(1): C346-57.

Wang P, Kumar P, Wang C, DeFea KA. Differential regulation of class IA phosphoinositide 3-kinase catalytic subunits p110 alpha and beta by protease-activated receptor-2 and beta-arrestins. Biochem J. 2007 Dec 1; 408(2): 221-30.

Zoudilova M, Kumar P, Ge L, Wang P, Bokoch GM, DeFea KA. Beta-arrestin-dependent regulation of the cofilin pathway downstream of protease-activated receptor-2. J Biol Chem. 007 Jul 13; 282(28): 20634-46.