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. 2006 Nov 7;103(46):17384–17389. doi: 10.1073/pnas.0600050103

Fig. 3.

Fig. 3.

SPL expression results in constitutive activation of p38. (A) Cells expressing SPL or vector control were treated with vehicle, pifithrin-α, or SB203580 (SB), alone and in combination with 12.5 μM etoposide, incubated for 24 h, and harvested, and total and phosphorylated p38 were determined in whole-cell extracts by immunoblotting. Actin serves as a loading control. (B) Cells were treated with vehicle (white bars), etoposide (black bars), or etoposide and SB203580 (gray bars) for 24 h and harvested, and caspase-2 activity was determined in whole-cell extracts. Each figure is representative of at least two separate experiments. ∗, P < 0.00005, for SPL untreated versus SPL plus etoposide; †, P < 0.00007, for SPL plus etoposide versus SPL plus etoposide and SB203580. (C) Cells were treated with etoposide with or without p53 and p38 inhibitors and incubated for 24 h, and caspase-3 activity was determined in whole-cell extracts. ∗, P < 0.006, for SPL versus SPL plus etoposide; †, P < 0.10, for SPL plus etoposide versus SPL plus etoposide and pifithrin-α; ‡, P < 0.009, for SPL plus etoposide versus SPL plus etoposide and SB203580. (D) Cells were simultaneously treated with etoposide and SB203580, PI3-kinase inhibitor LY294002 (LY), or MEK inhibitor PD98059 (PD), incubated for 24 h, and harvested, and caspase-3 activity was determined in whole-cell extracts.