Feyza Engin

The overarching goal of my lab is to decipher the mechanisms by which organisms establish cellular homeostasis in the presence of chronic inflammation and organelle stress, with the aim of discovering novel therapeutics to treat diabetes. We investigate the role of β-cell endoplasmic reticulum (ER) stress in the pathogenesis of type 1 diabetes (T1D) and have generated tissue-specific, inducible in vivo mouse models to elucidate the role of distinct arms (IRE1α, Xbp1, and Atf6) of the unfolded protein response (UPR) during T1D progression. Using an IRE1α β-cell-specific deletion mouse model, my lab recently made the striking discovery that loss of IRE1α in β-cells, prior to islet immune infiltration, leads to a transient β-cell dedifferentiation, which allows β-cells to escape immune-mediated destruction. More recently, we are interested in identifying how cellular stress impacts β-cell plasticity.