EXtENDINg beta cell survival by UPRegulating ATF4 translation.
review · Level V
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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.
Medical subject headings
- Activating Transcription Factor 4
- Insulin-Secreting Cells
- Peptides
- Protein Biosynthesis
- Receptors, Glucagon