Diabetes is a complex genetic disease with significant environmental components. While previous studies have identified numerous human genetic variants that are significantly associated with diabetes risk, the biological mechanisms through which they impact disease etiology and interact with diabetes-relevant cellular stresses (inflammatory stress, endoplasmic reticulum stress etc.) still remains incompletely understood. My research focuses on human pancreatic islets – mini-organs responsible for secreting hormones that regulate blood sugar levels - and utilizes high-throughput multi-omic approaches within an integrated computational framework to understand how these diabetes-associated variants (dys)regulate responses to cellular stresses and thereby contribute towards islet dysfunction.
