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. 2019 Jul 19;294(36):13366–13377. doi: 10.1074/jbc.RA119.008967

Figure 2.

Figure 2.

Adropin34–76 treatment enhanced AKT signaling in the liver. A and B, the phosphorylation levels of Ser473 in AKT and total AKT protein levels (n = 4) (A) and the phosphorylation levels of Ser9 in GSK 3β and total GSK 3β protein levels (n = 4–5) (B) were determined by Western blotting. In A, α-tubulin was used as the loading control. The same α-tubulin band was used as the loading control for the blot of total IRS1 (Fig. 1A) and the blots of pIKK (α/β) (Ser176/180) and total IKK (α/β) (Fig. S6). In B, GAPDH was used as the loading control. C, glycogen levels were determined and were normalized to tissue masses (n = 8). D, nuclear levels (n = 4–5) and whole-tissue level (n = 4) of FoxO1 were measured by Western blotting. Histone H3 was used as the loading control in the blot of nuclear lysates. The same histone H3 band was used as the loading control for the blots of (n)SREBP1c (Fig. 6A), (n)CRTC2 (Fig. 8B), and (n)NF-κB p65 (Fig. S6). GAPDH was used as the loading control in the blot of whole-tissue lysates. *, p ≤ 0.05, adropin versus vehicle. Error bars, S.E.