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. 2017 Dec 13;8:2103. doi: 10.1038/s41467-017-02282-w

Fig. 5.

Fig. 5

GAr-dependent induction of E2F1 is mediated via PI3Kδ. a Western blots show the expression of E2F1 in H1299 cells expressing the GAr or EV following treatment with indicated drugs for 8 h. Phosphorylated 4E-BP1 (P-4E-BP1) was used to show mTOR activity. b Western blots show E2F1 expression levels in cells expressing the GAr or control plasmid (EV), treated with the indicated concentrations of inhibitors of PI3K p110δ (CAL-101), p110γ (middle panel) and p110α (lower panel) subunits. c The effect of wortmannin and the PI3Kδ-specific inhibitor (CAL-101) on the phosphorylation of AKT (P-AKT) and 4E-BP1 (P-4E-BP1) in cells treated with 40 ng/ml of PDGF for 30 min in serum-free medium. d Western blots showing the effect of GAr on the phosphorylation of AKT and 4E-BP1. e Western blot showing the expression of E2F1 following 24 h treatment with siRNA against PI3Kδ. f Western blot showing the expression of E2F1 in cells expressing EV or GAr followed by general induction of PI3K activity using MgSO4 (20 mM) and LPS (1 µg), with, or without, CAL-101 (10 µM). Western blots represent n ≥ 3. Actin was used as a loading control.