FIGURE 6.

RAD deficient CMs show increased I_Ca–L and CaMKII activity. (A) Recording and identification of representative I_Ca–L from a series of step pulses between −50 mV to +60 mV from a holding potential of −80 mV. 200 nM nifedipine, a specific blocker of L-type voltage-gated Ca^{2 +} channels, blocked the current. (B) Histogram analysis showing that the cell membance capacity (pF) was larger in KO CMs than that in WT CMs. (C) Typical I_Ca–L recording from WT CMs (black traces) and KO CMs (red traces). (D) I-V curves I_Ca–L showing that I_Ca–L density was significantly increased in KO CMs (n = 9, respectively). (E) Western blot shows expression of protein related to calcium regulation in WT and KO CMs, respectively. (F) Quantification of protein expression normalized by GAPDH in WT and KO CMs. (G) Western blot shows expression of calcineurin A, CaMKIIδ and phosphorylated CaMKII (Thr286) in WT and KO CMs, respectively. (H) Quantification of protein expression normalized by GAPDH in WT and KO CMs. Data are expressed as means ± S.E.M. of three independent experiments. ns, not significant; *P < 0.05; ***P < 0.001; ****P < 0.0001.