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John Corbett is a Professor and Co-Director of the Pilot Feasibility Program at the UW Comprehensive Diabetes Center, University of Wisconsin–Madison. His research focuses on the mechanisms responsible for beta-cell dysfunction and damage in the development of diabetes. He utilizes molecular, biochemical, transgenic, and immunological approaches to unravel these mechanisms. Corbett's work seeks to understand how cytokines control beta-cell fate and response, specifically identifying how damaging aspects of cytokines interplay with protective pathways. Notably, he discovered that nitric oxide acts as a mediator of the inhibitory effects of IL-1 on insulin secretion in beta cells, highlighting that human islets can express inducible nitric oxide synthase (iNOS) and produce high levels of nitric oxide in vitro. His research has shown that locally produced IL-1 activated tissue macrophages can lead to beta-cell damage through a nitric oxide-dependent mechanism, with implications for both rodent and human islets. Furthermore, Corbett has pioneered studies that demonstrate the functional recovery of beta cells after cytokine-mediated damage, which involves new gene expression stimulated by nitric oxide. His investigations into the DNA damage response (DDR) have uncovered that the ATM kinase is responsible for triggering beta-cell apoptosis in response to cytokine treatment, positioning nitric oxide as a direct regulator of DDR in beta cells.
Department: Department of Computer Sciences