Kir2.1 potassium channels are the major determinants of IK1 in murine ventricular cardiomyocytes.19 In order to test if the decreased IK1 in dystrophic cardiomyocytes can be explained by a reduced expression of Kir2.1 channels, we performed western blot experiments with membrane fractions of cardiac ventricular tissues isolated from wt and dystrophic (mdx and mdx-utr) mice. Fig. 2 (A and B) shows that Kir2.1 protein levels in wt and dystrophic ventricles were similar. This suggests that Kir2.1 channel expression is normal in dystrophin-deficient cardiomyocytes. Finally, Fig. 2C compares typical Kir2.1 immunostainings of an isolated wt and a mdx cardiomyocyte. Cross-striations, typical for T-tubular localization of Kir2.1 channels in mouse ventricular cardiomyocytes,27 can be observed both in the normal and the dystrophic cell. Similar staining patterns showing cross-striations were obtained in all the studied wt and mdx cardiomyocytes, which were isolated from 3 normal and dystrophic mice, respectively. These immunostaining data implies normal T-tubular Kir2.1 channel localization in dystrophic cardiomyocytes. Figure 2.Kir2.1 protein exparession and localization in wt and dystrophic ventricular cardiomyocytes. (A) Representative western blot experiment of membrane lysates from adult wt and dystrophic (mdx and mdx-utr) ventricular tissues stained for Kir2.1 and the β-subunit of a Gs protein (AS7). The latter was used as loading control. (B) Relative band intensities of Kir2.1 normalized to the respective band intensities of the loading control plotted as means ± SEM for wt (n = 5) and dystrophic (mdx, n = 6; mdx-utr, n = 2) animals. A Student's t-test did not reveal a significant difference between wt and mdx (p = 0.11; n.s., not significant). (C) Typical examples of Kir2.1 immunostainings of an isolated wt (left) and mdx (right) cardiomyocyte.