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. 2021 May 27;297(1):100836. doi: 10.1016/j.jbc.2021.100836

Figure 6.

Figure 6

Rate of force redevelopment (ktr) was elevated by mutant hS2 proteins in fibers expressing cMyBP-C DDD in transgenic (Tg) protein.A, raw ktr traces and B, values for fibers that expressed cMyBP-C AAA without treatment (black) and fibers treated with 9 μM hS2Wt (green), hS2R870H (blue), hS2E924K (orange), and hS2E930Δ (red) proteins. C, raw ktr traces and D, values for fibers that expressed cMyBP-C DDD without treatment (black) and treated with 9 μM hS2Wt (green), hS2R870H (blue), hS2E924K (orange), and hS2E930Δ (red) proteins. Statistical analyses were performed by one-way ANOVA, and Tukey’s pooled multiple variance test was used to calculate the significance between the ktr values. n = 5 fibers/3 mice (12 weeks old, FVB/N, mixed sex), where n is each fiber treated with a single concentration of myosin S2 protein and measured ktr at submaximal pCa 5.7 and sarcomere length 2.0 μM. Data are expressed as the mean ± SEM. See Table 5 for analysis of main factors and interactions. ∗∗p < 0.01, and ∗∗∗p < 0.001 versus untreated controls. AAA, phospho-ablated cMyBP-C or phospho-ablation; cMyBP-C, cardiac myosin-binding protein-C; DDD, phospho-mimetic cMyBP-C; hS2E924K, human recombinant proximal S2 protein with E924K mutation; hS2E930Δ, human recombinant proximal S2 protein with E930Δ mutation; hS2R870H, human recombinant proximal S2 protein with R870H mutation; hS2Wt, human recombinant proximal S2 WT protein; S2, subfragment 2 region.