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. 2003 Sep 19;100(20):11624–11629. doi: 10.1073/pnas.1931483100

Fig. 1.

Fig. 1.

Insulin decreases Foxa-2 activity via PI3-kinase–Akt activation. (A) HepG2 cells were transfected with an expression vector for Foxa-2 and pPEPCK-Luc (gray bars) or p6xCdx-TkLuc (black bars). Cells were treated with 100 nM insulin, 10 μM LY294002, or 10 μM PD98059 alone or in combination. (B) HepG2 cells were transfected with p6xCdx-TkLuc. Cells were treated with insulin, 10 μM LY294002, or 10 μM PD98059 at the indicated concentrations, alone or in combination. (C) RT-PCR analysis of Foxa-1–3 and target genes. Primary hepatocytes were grown in the absence and presence of 50 nM insulin, LY294002, and PD98059 for 6 h before gene expression analysis. (D) HepG2 cells were transfected with an expression vector for Foxa-1, Foxa-2, Akt, or AktK179A alone or in combination. p6xCdx-TkLuc was used as reporter gene. In all experiments luciferase activity was normalized to β-galactosidase activity. All vectors were transfected at 125 ng. Values are mean of six independent experiments ± SD. *, P ≤ 0.01; **, P ≤ 0.001.