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. Author manuscript; available in PMC: 2021 Nov 25.
Published in final edited form as: Basic Res Cardiol. 2020 Nov 25;115(6):71. doi: 10.1007/s00395-020-00834-8

Fig. 7.

Fig. 7

CaMKII activation via S280 O-GlcNAcylation regulates IK1 and Ito recovery in hyperglycemia. a Representative voltage-gated K+ currents and IK1 traces in normoglycemia and hyperglycemia in CaMKIIδ-knockout (KO), overexpression (OE) and O-GlcNAc-resistant S280A knock-in mouse myocytes. bj K+ current remodeling in CaMKIIδ-KO and OE in normoglycemia. CaMKIIδ-S280A had a normal baseline phenotype. Hyperglycemia effects on Ito recovery kinetics (f, g) and IK1 (h, i) but not on Ito amplitude (b) were prevented in both CaMKIIδ-KO and S280A. Two-way ANOVA; *p < 0.05, **p < 0.01, ***p < 0.001 vs. normoglycemia; p < 0.05, ††p < 0.01, †††p < 0.001 vs. WT control