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. 2009 Apr 17;284(16):10764–10773. doi: 10.1074/jbc.M809116200

FIGURE 2.

FIGURE 2.

Inhibitors of the PI3K/Akt signaling module do not inhibit the activation of Akt by GIP. A, INS-1 cells were pretreated with dimethyl sulfoxide (DMSO; control) or inhibitors of PI3K signaling (15 μm LY294002 or 5 μm Akt VIII) and then treated with ±10 nm GIP or 10 nm IGF-I for 15 min. Western analysis and Akt KA assays were performed on cell lysates with indicated antibodies. IP, immunoprecipitate. B and C, shown is the mean change ± S.E. in Akt activity (P-GST-GSK3/Akt) relative to DMSO control (n = 4) for GIP- (B) and IGF-I-treated (C) cells. #, p < 0.05 versus DMSO control; $, p < 0.05 versus IGF-I without inhibitor. D, mouse islets were pretreated with DMSO (control) or 15 μm LY294002 and then treated with ±10 nm GIP for 15 min. Western analysis and Akt KA assays were performed with indicated antibodies. E, shown is the mean change ± S.E. in Akt activity relative to DMSO control (n = 3). #, p < 0.05 versus DMSO control. Anti-β-actin and anti-GST (GST-GSK3) blots were internal controls.