EXtENDINg β cell survival by UPRegulating ATF4 translation

Ronald C. Wek, Tracy G. Anthony

Research output: Contribution to journalShort survey

9 Scopus citations

Abstract

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
Volume4
Issue number5
DOIs
StatePublished - Nov 1 2006

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

Fingerprint Dive into the research topics of 'EXtENDINg β cell survival by UPRegulating ATF4 translation'. Together they form a unique fingerprint.

  • Cite this