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. Author manuscript; available in PMC: 2022 Feb 5.
Published in final edited form as: Circ Res. 2020 Dec 2;128(3):335–357. doi: 10.1161/CIRCRESAHA.120.316738

Fig. 2.

Fig. 2.

A: Immunoblots of cardiac pSer256-FOXO1, total FOXO1, pSer473-AKT and total AKT and PonceauS staining in non-diabetic and diabetic C57BL/6 mice, 12 weeks post-STZ administration (analysis shown in Online Figure III-A). B: Immunoblots of pSer473-AKT, total AKT, KLF5 and β-ACTIN proteins from control and insulin-stimulated AC16 cells (analysis shown in Online Figure IV-A). C: Immunoblots of total FOXO1, pSer256-FOXO1 and β-ACTIN proteins from AC16 cells treated with adenoviruses expressing GFP, wtFOXO1 or caFOXO1 without (analysis shown in Online Figure IV-C) or with insulin treatment. D: Immunoblots of KLF5 and β-ACTIN proteins from AC16 cells treated with adenoviruses expressing GFP and wtFOXO1 without or with insulin stimulation (analysis shown in Online Figure IV-F). E: Immunoblots of pSer473-AKT, total AKT, KLF5 and β-ACTIN proteins from AC16 cells treated with adenovirus expressing caFOXO1 (analysis shown in Online Figure IV-G) without or with insulin treatment. F: FOXO1 enrichment in KLF5 promoter sequence fragments precipitated with FOXO1 antibody from AC16 cells expressing GFP or wtFOXO1. G:FOXO1 enrichment in KLF5 promoter sequence fragments precipitated with FOXO1 antibody from AC16 cells expressing wtFOXO1 and treated with insulin. H: Luciferase activity normalized to firefly from AC16 cells transfected with plasmids containing the wild type KLF5 −1757/−263bp promoter fragment (pGL3BV-wt-hKLF5) or the mutant [-1757/-263bp](-342/-317bp)N→A (pGL3BV-mut-hKLF5) and infected with adenoviruses expressing GFP or wtFOXO1.