EXtENDINg β cell survival by UPRegulating ATF4 translation

Ronald C. Wek, Tracy G. Anthony

Research output: Contribution to journalShort survey

9 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)333-334
Number of pages2
JournalCell Metabolism
Issue number5
StatePublished - Nov 1 2006

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

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