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. 2014 Mar;184(3):819–826. doi: 10.1016/j.ajpath.2013.11.021

Figure 4.

Figure 4

Streptozotocin treatment alters the IR/PI3K/AKT pathway in Ntg and tauKO mice. A: Immunoblot analyses of pIR, IR, pPI3k(p85), PI3k, pAKT(Ser473), AKT, GSK3β (Ser9), and GSK3β of protein extracts from whole-brain homogenates of Ntg, Ntg-STZ, tauKO, and tauKO-STZ mice at 5 months of age are shown on alternating lanes. B: Quantification normalized to GAPDH and expressed as percentage of control. Pairwise comparisons: ∗P < 0.05, ∗∗P < 0.01 for phosphorylated IR (Ntg-STZ, 31.8% ± 5.1%; tauKO-STZ, 20.2% ± 7.2%; two-way analysis of variance: genotype [F(1,10) = 2.23], treatment [F(1,10) = 20.03, P < 0.01], interaction [F(1,10) = 0.43]) and phosphorylated PI3K (Ntg-STZ, 14.3% ± 8.0%; tauKO-STZ, 18.9% ± 3.0%). Two-way analysis of variance: genotype [F(1,11) = 0.11], treatment [F(1,11) = 9.93, P < 0.01], interaction [F(1,10) = 0.45]. Phosphorylated AKT at residue Ser473 (Ntg-STZ, 26.3% ± 6.0%; tauKO-STZ, 13.5% ± 4.5%; two-way analysis of variance: genotype [F(1,10) = 2.78], treatment [F(1,10) = 17.12, P < 0.01], interaction [F(1,10) = 0.42]) and GSK3β-Ser9 (NTg-STZ, 30.4% ± 6.0%; tauKO-STZ, 24.7% ± 5.0%; two-way analysis of variance: genotype [F(1,12) = 0.53], treatment [F(1,12) = 27.83, P < 0.001], interaction [F(1,12) = 0.10]). The values represent the means ± SEM. MW, molecular weight.