Table 2.
Control | (100) |
GH alone | 177 ± 12 |
GH + chelerythrine HCl (5 μM) | 173 ± 10 |
GH + PD 98059 (20 μM) | 186 ± 14 |
GH + wortmannin (50 nM) | 106 ± 6 |
GH + LY 294002 (2 μM) | 107 ± 12 |
GH + rapamycin (10 nM) | 88 ± 10 |
GH + actinomycin D (4 μg/ml) | 180 ± 18 |
JAK2 antisense | 68 ± 3 |
GH + JAK2 antisense | 73 ± 10 |
JAK-2 scrambled | 96 ± 14 |
GH + JAK-2 scrambled | 179 ± 5 |
Δ p85 PI3 kinase | 104 ± 3 |
GH + Δ p85 PI3 kinase | 90 ± 10 |
Activated p70 S6 kinase | 143 ± 10 |
Activated p70 S6 kinase + rapamycin | 153 ± 7 |
GH + activated p70 S6 kinase | 189 ± 14 |
Wild-type p70 S6 kinase | 95 ± 11 |
GH + wild-type p70 S6 kinase | 167 ± 12 |
GH + wild-type p70 S6 kinase + rapamycin | 97 ± 12 |
These data describe changes in the immunoprecipitated PDE4A activity of F442A cells. Identical numbers of cells were analyzed under conditions where all the PDE4A was immunoprecipitated. Data are means ± SD for n = 5 experiments. Basal PDE4A activity in the immunoprecipitates was 2.1 ± 0.1 pmol/min/mg of protein. Total rolipram-inhibited PDE4 activity was 4.5 ± 0.9 pmol/min/mg of protein. Total cilostimide-inhibited PDE3 activity was 3.3 ± 0.2 pmol/min/mg of protein. Changes in PDE4A activity are given relative to control set at 100%. Cells were treated with ligands for 30 min.