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. Author manuscript; available in PMC: 2022 Apr 1.
Published in final edited form as: Kidney Int. 2020 Dec 13;99(4):870–884. doi: 10.1016/j.kint.2020.10.038

Figure 1. Ischemia reperfusion induced acute translocation and activation of AKT1 in renal mitochondria.

Figure 1.

After ischemia, kidneys were harvested at various time points during reperfusion. (A) Increase in AKT1 and pAKT1 in mitochondria following reperfusion. Mitochondrial fractions were isolated and protein lysates were analyzed by western blotting with antibodies for total pAKT1, AKT1, mitochondria marker VDAC and cytosol marker actinin. (B) Mitochondrial AKT1 is increased following reperfusion graph (Kruskall-Wallis test, p<0.05). (C) Renal sections from the sham control or 1 hour after IRI was used to visualize AKT1 phosphorylation in tubules with immunohistochemistry staining. (D) Increased pAKT positive areas (%) 1 hour after IRI (p<0.001, n=13 in each group). (E) Co-localization of pAKT1 with renal tubule mitochondria 60 min post-ischemia. Renal sections were stained with pAKT1 (S473) antibodies and Mitotracker Green.