FIGURE 7.

GIP-mediated suppression of p38 MAPK and JNK also promotes the survival of INS-1 cells exposed to ER and genotoxic stress. A, INS-1 cells were treated without or with STS (100 nm), thapsigargin (500 nm), or etoposide (5 μm) ± 10 nm GIP for 4 h, and Western analysis was performed on total cell lysates with the indicated antibodies. Shown are representative blots of at least three independent experiments. Anti-β-actin blot was an internal control. B, INS-1 cells were treated without or with STS, thapsigargin, or etoposide ± GIP for 6 h, and cell death was determined (mean ± S.E. of cell death (n = 6); #, p < 0.05 as indicated). C, INS-1 cells were treated without or with STS, thapsigargin, or etoposide ± p38i (5 μm) or JNKi (5 μm) for 6 h, and cell death was determined (mean ± S.E. of cell death (n = 6); #, p < 0.05 versus STS only; $, p < 0.05 versus thapsigargin only; %, p < 0.05 versus etoposide only).