The decrease in the maximal actomyosin-S1-ATPase activity of mutant filaments in the presence of levosimendan was highly significant when compared to treated wild type filaments (TF-G34S Δy max = −0.115, TF-D127Y Δy max = −0.078) ( Table 2 , Figure 8 C).
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De Novo Missense Mutations in <i>TNNC1</i> and <i>TNNI3</i> Causing Severe Infantile Cardiomyopathy Affect Myofilament Structure and Function and Are Modulated by Troponin Targeting Agents.
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