This dissertation investigates the relationship between structure and function of ATP‑sensitive potassium (KATP) channels in pancreatic cells. Mutations in KATP channel proteins can disrupt normal channel activity by altering gating or trafficking mechanisms. By examining the molecular effects of these mutations, this work advances understanding of how KATP channel structure governs function. These insights contribute to a clearer understanding of islet dysfunction and may support the development of targeted therapies aimed at improving KATP channel regulation.
