Fig. 4

DGK inhibition activates ERK1/2 signaling in a time-dependent manner. Human ASM cells were treated with vehicle or DGK I (20 µM) for 0, 5, 10, 15 and 30 min. Cells were lysed and immunoblotted for ERK1/2 phosphorylation and β-actin (A). Graphical representation of mean ± SEM (n = 3 distinct donors) for ERK1/2 phosphorylation (B). The densitometry data for ERK1/2 phosphorylation by DGK I were normalized to matched vehicle-treated controls at each time point, and graphed as fold change from the basal. *p < 0.05 (compared to vehicle basal) using one-way-ANOVA with Bonferroni post-hoc analysis. Please note that the gel images shown are cropped from the full length images