Figure 3

Proposed Model of PSP/reg in the ER stress response. ER stress either via genetic (loss of WFS1) or environmental (treatment with tunicamycin or thapsigargin), results in homeostatic alterations in the ER. In turn, this results in increased expression, translation, and secretion of PSP/reg. PSP/reg likely exerts its downstream effects in both an autocrine and paracrine manner. We hypothesize that PSP/reg likely counterbalances the effects of ER stress by simultaneously promoting beta cell proliferation and pro-survival pathways.