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EXtENDINg beta cell survival by UPRegulating ATF4 translation
Journal article   Open access  Peer reviewed

EXtENDINg beta cell survival by UPRegulating ATF4 translation

Ronald C Wek and Tracy G Anthony
Cell metabolism, Vol.4(5), pp.333-334
11/2006
DOI: https://doi.org/10.1016/j.cmet.2006.10.006
PMID: 17084705

Abstract

Insulin-Secreting Cells - physiology Protein Biosynthesis Cell Survival Peptides - physiology Activating Transcription Factor 4 - genetics Receptors, Glucagon - metabolism Protein Folding Hypoglycemic Agents - pharmacology Peptides - pharmacology Up-Regulation - drug effects Animals Activating Transcription Factor 4 - metabolism Glucagon-Like Peptide-1 Receptor Insulin-Secreting Cells - drug effects Mice Venoms - pharmacology Receptors, Glucagon - physiology
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.
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https://doi.org/10.1016/j.cmet.2006.10.006View
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