EXtENDINg β cell survival by UPRegulating ATF4 translation

Citations of this article
Mendeley users who have this article in their library.


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

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free