Table 2.
Differential effects of kinase inhibitors on long-term IGF-1 stimulated AAH immunoreactivity
IGF-1 Stimulation | Kinase Inhibitor | IGF-1 × Inhibitor | ||||
---|---|---|---|---|---|---|
Inhibitor | F-Ratio | P-Value | F-Ratio | P-Value | F-Ratio | P-Value |
H-89 | 16.95 | 0.083 | 0.21 | N.S. | 25.81 | 0.016 |
PD98059 | 11.84 | 0.0003 | 49.81 | <0.0001 | 24.42 | <0.0001 |
LiCl | 75.57 | <0.0001 | 3.69 | 0.071 | 8.92 | 0.0008 |
Go6983 | 9.09 | <0.0001 | 79.37 | <0.0001 | 6.42 | <0.0001 |
TBCA | 53.54 | <0.0001 | 13.55 | <0.0001 | 9.18 | 0.032 |
Huh7 human hepatoma cells grown in 96-well micro-cultures were pre-treated with vehicle (control), LiCl, TBCA, Gö6983, H-89, or PD98059 to inhibit GSK-3β, CK2, pan-PKC, PKA, or MEK, and then stimulated for 60 minutes with 10 ng/ml IGF-1. Cellular ELISAs measured immunoreactivity to AAH (A85G6-C-terminus; A85E6 and FB50-N-terminus) and β-actin. Data were analyzed by Two-way ANOVA. Corresponding graphs with post-hoc Fisher LSD results are shown in Figure 6.