CD59 is a cell surface protein that protects cells against the body’s immune system, and glycation is a process by which proteins react with sugar, inactivating their function. In diabetes patients, elevated blood glucose levels cause CD59 on endothelial cells to undergo glycation and lose their function, resulting in higher rates of vascular injury. Although wildtype CD59 is prone to glycation, one CD59 mutant has been shown to be immune to glycation yet functional. The goal of this project is to characterize the functionality, glycation-resistance, and therapeutic effects of various CD59 mutants that can be produced using base-editing technology. Identified functional and glycation-resistant CD59 mutants have the potential to reduce vascular injury in diabetes patients in the clinic.

Novel drug delivery and genome-editing methods have the power to treat disease and the SuperUROP program allows me to be at the cutting-edge of their development. During my time at the Langer Lab, I have aided in the development of various nanoparticle formulations for drug delivery and I am excited to apply this knowledge to my SuperUROP work. The project has the potential to improve the lives of diabetes patients, which excites me tremendously.