EXtENDINg beta cell survival by UPRegulating ATF4 translation
- PMID: 17084705
- DOI: 10.1016/j.cmet.2006.10.006
EXtENDINg beta cell survival by UPRegulating ATF4 translation
Abstract
In this issue of Cell Metabolism, Daniel Drucker and colleagues (Yusta et al., 2006) explore how the incretin mimetic exendin-4 improves beta 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.
Comment on
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GLP-1 receptor activation improves beta cell function and survival following induction of endoplasmic reticulum stress.Cell Metab. 2006 Nov;4(5):391-406. doi: 10.1016/j.cmet.2006.10.001. Cell Metab. 2006. PMID: 17084712
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