通过上调ATF4翻译来延长β细胞存活时间。
EXtENDINg beta cell survival by UPRegulating ATF4 translation.
作者信息
Wek Ronald C, Anthony Tracy G
机构信息
Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.
出版信息
Cell Metab. 2006 Nov;4(5):333-4. doi: 10.1016/j.cmet.2006.10.006.
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.
在本期《细胞代谢》中，丹尼尔·德鲁克及其同事（尤斯塔等人，2006年）探讨了肠促胰岛素类似物艾塞那肽-4如何在内质网应激期间改善β细胞功能和存活。他们的研究结果表明，由胰高血糖素样肽-1受体激活引发的蛋白激酶A信号传导差异性地调节未折叠蛋白反应（UPR）的一个分支。对这条UPR途径的调节导致转录因子ATF4的翻译表达增强，ATF4是应激补救和细胞存活的关键转录因子。
Zotero 插件