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. 2021 May 20;153(7):e202012801. doi: 10.1085/jgp.202012801

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© 2021 Sitbon et al.

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Figure 3. — Myosin RLC, cMyBP-C, and TnI phosphorylation in ventricular CMFs purified from the hearts of WT, HCM-A57G, RCM-E143K, and Δ43 mice. The hearts of 4 M and 3 F (7.5–10-mo-old) WT-ELC, 3 M and 5 F (8–10-mo-old) A57G, 3 M and 3 F (6–9-mo-old) E143K, and 4 M and 2 F (7.5–10-mo-old) Δ43 mice were used. (A) SDS-PAGE and sarcomeric protein phosphorylation monitored by ProQ/Coomassie. (B) Quantification of myosin RLC, cMyBP-C, and TnI phosphorylation in CMFs from all genotypes. Open symbols depict female mice and closed symbols depict male mice. Data are mean ± SD and were analyzed using one-way ANOVA with Tukey’s comparison test with significance depicted as *, P < 0.05 between mutant versus WT; $$$, P < 0.001 for A57G versus E143K; and &, P < 0.05 for E143K versus Δ43 mice. Abbreviations: +P-RLC, phosphorylated form of mouse ventricular RLC; +P-MyBP-C, phosphorylated form of mouse cMyBP-C; +P-TnI, phosphorylated form of TnI; F/A, F-actin; ELC_mse, mouse ventricular essential light chain; ELC_hu, human transgenic ELC; Δ43 ELC, N-terminally truncated ELC protein standard.