Corrigendum: IRS1 deficiency protects β-cells against ER stress-induced apoptosis by modulating sXBP-1 stability and protein translation
نویسندگان
چکیده
“Ca2+ in cytosol was measured using Fura-2 and Ca2+ in ER was measured using FRET-based probe D1ER cameleon in the basal state and after thapsigargin stimulation (100 nM for 1000 sec). Representative Ca2+ measurements in cytosol and ER (left panel). Quantitative ER Ca2+ levels of the average value prior to thapsigargin stimulation (Basal) and the minimum value after addition of thapsigargin (Tg(+ )) (right panel). Data are means ± SEM, n = 43 for control, n = 50 for IRS1KO, and n = 40 for IRS2KO β -cells. *P < 0.05, **P < 0.01”.
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IRS1 deficiency protects β-cells against ER stress-induced apoptosis by modulating sXBP-1 stability and protein translation
Endoplasmic reticulum (ER) stress is among several pathological features that underlie β-cell failure in the development of type 1 and type 2 diabetes. Adaptor proteins in the insulin/insulin-like-growth factor-1 signaling pathways, such as insulin receptor substrate-1 (IRS1) and IRS2, differentially impact β-cell survival but the underlying mechanisms remain unclear. Here we report that β-cell...
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