Forskolin-induced increase of PARP-1 and pADPr requires the ERK pathway.

<p>Left column (A, C, E): Representative Western blots used for quantification shown in right column (B, D, F). Phosphorylation of the ERK pathway substrate S6K was used as a stimulation-dependent positive control quantified as the ratio of p-S6K to total S6K (A, B). Histone 2B was used as a loading control (C, E). Fsk treatment (black bar) produced an increase of p-S6K, PARP-1, and pADPr (B, D, and F, respectively). The Fsk induced increase was prevented by the ERK inhibitor U0126 (grey bar; B, D, F). The inhibitor alone had no effect on PARP-1 or pADPr levels (striped bar; D, F respectively) compared with basal controls (white bar; D, F). Student's t-test (B,D,F); * = p<0.05; ** = p<0.01; NS = not significant.