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. 2010 Feb 9;5(2):e9135. doi: 10.1371/journal.pone.0009135

Figure 2. Thapsigargin inhibits APP proteolysis and induces ER stress UPR signaling.

Figure 2

Increasing doses of thapsigargin inhibits γ-secretase cleavage of APPGV16 (top graph). Titrated doses of thapsigargin induced graded increases in UPR stress signaling through phospho-PERK (pPERK blot) and phospho-eIF2α (p-eIF2 α), beginning at 0.1 µM and reaching a plateau at 0.5 µM thapsigargin. The increases in UPR signaling correlate with the levels of phospho-p38 (pp38 blot) and phospho-JNK (pp54/JNK, pp46JNK blot), as maximal stimulation is observed in the same concentration range. Total protein expression levels remain unchanged, as eIF2α and APPGV16 protein levels were consistent across treatment conditions.