EXtENDINg beta cell survival by UPRegulating ATF4 translation.
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.
Wek
Ronald C
RC
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
Anthony
Tracy G
TG
D051701:Activating Transcription Factor 4 / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002470:Cell Survival; D000077270:Exenatide; D000067757:Glucagon-Like Peptide-1 Receptor; D007004:Hypoglycemic Agents / Q000494:pharmacology; D050417:Insulin-Secreting Cells / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D010455:Peptides / Q000494:pharmacology / Q000502:physiology*; D014176:Protein Biosynthesis; D017510:Protein Folding; D018027:Receptors, Glucagon / Q000378:metabolism* / Q000502:physiology; D015854:Up-Regulation / Q000187:drug effects; D014688:Venoms / Q000494:pharmacology
C497109:ATF4 protein, human; C000593833:GLP1R protein, human; C000593834:Glp1r protein, mouse; D000067757:Glucagon-Like Peptide-1 Receptor; D007004:Hypoglycemic Agents; D010455:Peptides; D018027:Receptors, Glucagon; D014688:Venoms; D051701:Activating Transcription Factor 4; D000077270:Exenatide