EXtENDINg beta cell survival by UPRegulating ATF4 translation

Cell Metab. 2006 Nov;4(5):333-4. doi: 10.1016/j.cmet.2006.10.006.

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.

Publication types

  • Review
  • Comment

MeSH terms

  • Activating Transcription Factor 4 / genetics
  • Activating Transcription Factor 4 / metabolism*
  • Animals
  • Cell Survival
  • Exenatide
  • Glucagon-Like Peptide-1 Receptor
  • Hypoglycemic Agents / pharmacology
  • Insulin-Secreting Cells / drug effects
  • Insulin-Secreting Cells / physiology*
  • Mice
  • Peptides / pharmacology
  • Peptides / physiology*
  • Protein Biosynthesis*
  • Protein Folding
  • Receptors, Glucagon / metabolism*
  • Receptors, Glucagon / physiology
  • Up-Regulation / drug effects
  • Venoms / pharmacology

Substances

  • ATF4 protein, human
  • GLP1R protein, human
  • Glp1r protein, mouse
  • Glucagon-Like Peptide-1 Receptor
  • Hypoglycemic Agents
  • Peptides
  • Receptors, Glucagon
  • Venoms
  • Activating Transcription Factor 4
  • Exenatide