Fig. 1: Thapsigargin and Tunicamycin treatment induce robust ER stress and cell death in pancreatic β cells. | Cell Death Discovery

Fig. 1: Thapsigargin and Tunicamycin treatment induce robust ER stress and cell death in pancreatic β cells.

From: ER stress-induced cell death proceeds independently of the TRAIL-R2 signaling axis in pancreatic β cells

Fig. 1

A, B Dose-dependent death kinetics of Min6 and Ins1E cells after stimulation with Thapsigargin (TG) or Tunicamycin (TM). Kinetic analyses in high response scenarios were terminated once cell detachment and cell loss made readouts unreliable. All data are from n = 3 independent experiments and mean ± SEM. C, D EC50 determination from response data shown in A and B. EC50 values were derived from endpoint readings at 42 h or for TM treated Ins1E cells at 62 h of treatment. E, F Protein amounts of BIP and CHOP after treatment with TG, TM or DMSO were determined by immunoblotting. Vinculin served as loading control. Min6 cells were treated with 0.15 µM TG or 0.35 µg/ml TM. Ins1E cells were treated with 0.025 µM TG or 0.125 µg/ml TM.

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