Stress Sensing in the Endoplasmic Reticulum
Our research is focused on the mechanisms of stress sensing in the endoplasmic reticulum (ER) via the unfolded protein response (UPR) pathways. The UPR not only is key for development of secretory tissues, but —when excessively activated— also causes disease, e.g. diabetes. The overall goal is to understand how proximal UPR sensing and signaling compare between the ER stress driven UPR, the adaptive UPR in secretory cell development, and the maladaptive UPR in disease. A background in development of in vivo biosensors for UPR activation and in studying B to plasma cell differentiation as well as collaborations within the institute provide the expertise and models to dissect what tips the balance in the transition of an adaptive to a maladaptive UPR that we, ultimately, aim to reverse.