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Dilated cardiomyopathy (DCM) is the third most common cause of heart failure and the primary reason for heart transplantation; upward of 70% of DCM cases are considered idiopathic. Our in-vitro experiments showed that reduced hybrid/complex N-glycosylation in mouse cardiomyocytes is linked with DCM. Further, we observed direct effects of reduced N-glycosylation on K v gating. However, it is difficult to rigorously determine the effects of glycosylation on K v activity, because there are multiple K v isoforms in cardiomyocytes contributing to the cardiac excitation. Due to complex functions of K v isoforms, only the sum of K + currents (I Ksum ) can be recorded experimentally and decomposed later using exponential fitting to estimate component currents, such as I Kto , I Kslow , and I Kss . However, such estimation cannot adequately describe glycosylation effects and K v mechanisms. Here, we propose a framework of simulation modeling of K v kinetics in mouse ventricular myocytes and model calibration using the in-vitro data under normal and reduced glycosylation conditions through ablation of the Mgat1 gene (i.e., Mgat1KO). Calibrated models facilitate the prediction of K v characteristics at different voltages that are not directly observed in the in-vitro experiments. A model calibration procedure is developed based on the genetic algorithm. Experimental results show that, in the Mgat1KO group, both I Kto and I Kslow densities are shown to be significantly reduced and the rate of I Kslow inactivation is much slower. The proposed approach has strong potential to couple simulation models with experimental data for gaining a better understanding of glycosylation effects on K v kinetics.