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. 2022 Sep 24;298(11):102532. doi: 10.1016/j.jbc.2022.102532

Figure 3.

Figure 3

C-terminal CX3CL1 fragment (CX3CL1-ct) overexpression in transgenic mice induces insulin/IGF-1 signaling pathways.A, neuron-specific overexpression of CX3CL1-ct in mice was achieved by breeding CX3CL1-ct mice with CaMKIIa-Tet mice. The transgene was turned on by doxycycline withdrawal at P45. Hippocampal and cortical protein lysates from the indicated genotypes of mice were examined with indicated antibodies by Western blotting. CX3CL1-ct/tTa mice had significantly increased expression of insulin receptor (anti-IGFβ) and insulin growth factor-1 (IGF-1) receptor (IGF-1R; detected by anti-IGF-1Rβ). Downstream molecules insulin substrate 1 (IRS1) and IRS2, Akt, PDK1, and Foxo3 were more obviously activated. B, bar graphs show comparative levels normalized to the loading control. N = 3 independent experiments (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001, one-way ANOVA). IGF, insulin growth factor; P45, postnatal day 45.