In this issue of Cell Metabolism, Daniel Drucker and colleagues (Yusta et al., 2006) explore how the incretin mimetic exendin-4 improves β cell function and survival during ER stress. Their findings suggest that protein kinase A signaling elicited by GLP-1 receptor activation differentially modulates one arm of the unfolded protein response (UPR). Regulation of this UPR pathway leads to enhanced translational expression of ATF4, a transcription factor central for stress remedy and cell survival. © 2006 Elsevier Inc. All rights reserved.
Wek, R. C., & Anthony, T. G. (2006, November). EXtENDINg β cell survival by UPRegulating ATF4 translation. Cell Metabolism. https://doi.org/10.1016/j.cmet.2006.10.006