EXtENDINg β cell survival by UPRegulating ATF4 translation

Ronald C. Wek, Tracy G. Anthony

Research output: Contribution to journalShort survey

9 Citations (Scopus)

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

Fingerprint

Unfolded Protein Response
Cell Survival
Activating Transcription Factor 4
Incretins
Cyclic AMP-Dependent Protein Kinases
Glucagon-Like Peptide-1 Receptor
exenatide

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology

Cite this

EXtENDINg β cell survival by UPRegulating ATF4 translation. / Wek, Ronald C.; Anthony, Tracy G.

In: Cell Metabolism, Vol. 4, No. 5, 01.11.2006, p. 333-334.

Research output: Contribution to journalShort survey

Wek, Ronald C. ; Anthony, Tracy G. / EXtENDINg β cell survival by UPRegulating ATF4 translation. In: Cell Metabolism. 2006 ; Vol. 4, No. 5. pp. 333-334.
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