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My lab has two major projects: 1) To understand the connections between ER stress and apoptosis of pancreatic islet b-cells. This will inform us whether protein misfolding is central to development of type 2 diabetes, and may in turn lead to new therapeutic targets for treating this disease. 2) To identify and develop novel small molecule effectors of key regulators of pathways which reverse ER stress, such as the unfolded protein response (UPR). In this regard, the unfolded protein response (UPR) signaling protein Ire1 presents an attractive druggable target because we have already shown that occupancy of Ire1?s kinase domain with small adenosine nucleotide-like drugs can trigger the entire UPR pathway.