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. 2007 Apr 2;104(15):6454–6459. doi: 10.1073/pnas.0610324104

Fig. 6.

Fig. 6.

PC2 modulates the kinetics of Ca2+ transient from RyR2. (a) Representative traces of Ca2+ transient in Pkd2+/+ and Pkd2−/− cardiomyocytes. Cardiomyocytes were loaded with fluo-4, and Ca2+ transients were then elicited by 20 mM caffeine in the absence of extracellular Ca2+. (b) Comparison of the Ca2+ transient. Shown are F/F0 in Pkd2+/+ (n = 32) and Pkd2−/− (n = 40) cardiomyocytes. Statistical significance was calculated by using a one-tailed t test: ∗∗, P < 0.001. (c) Rate of rise of Ca2+ transient in Pkd2+/+ and Pkd2−/− cardiomyocytes. Pkd2−/− cardiomyocytes have significantly decreased peak in fluorescence compared with Pkd2+/+ cardiomyocytes: ∗∗, P = 0.001 (one-tailed t test). (d) Duration of Ca2+ transient in Pkd2+/+ and Pkd2−/− cardiomyocytes. Pkd2−/− cardiomyocytes had a significantly longer duration of Ca2+ transients compared with Pkd2+/+. Statistical significance was calculated by using a one-tailed t test: ∗∗, P < 0.001 (number of experiments for each genotype: 35).

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