I began my post as a Postdoctoral Fellow (PDF) in November 2011 in the lab of Professor Sasanka Ramanadham, at the University of Alabama at Birmingham (UAB), in the School of Medicine, Department of Cell, Integrative and Developmental Biology (CDIB), Comprehensive Diabetes Center (CDC). Professor Ramanadham’s work was also in fatty acids and β-cell apoptosis but in a type 1 diabetes (T1D) setting. The group has identified mechanisms by which the Ca2+-independent phosphlipase A2 (iPLA2β) enzyme in pancreatic β-cells plays a role in ER stress-induced β-cell apoptosis. Two of my current projects are focused on (1) specific targets in the salvage and de novo ceremide generating pathways as this has not been explored in the context of pancreatic cell and islet iPLA2β involvement and (2) unveiling the intricacies of the cellular inflammatory process, specifically the NFκB pathway as intriguingly there are no reported links between iPLA2β and NFκB in terms of T1DM progression.
This is particularly exciting for me as a pharmacologist identifying novel therapeutic targets, and drug therapy development, for diabetes as I recently characterized a new characterized iPLA2β-specific inhibitor FKGK18, which is more potent, more specific, and less toxic, than other iPLA2β inhibitors in vitro and exerts many immunologically beneficial effects in vivo (under revision) which I intend to use for my upcoming projects.