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Overview
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MYLK3 (or myosin light chain kinase 3) plays a key role in rate of cross-bridge recruitment in cardiac myocytes. MYLK3 is upregulated in failing human myocardia and expression of MYLK3 correlates with the pulmonary arterial pressure of patients with heart failure. Knockdown of MYLK3 with small interfering RNAs in cultured rat cardiomyocytes decreases Myl2 phosphorylation and impairs epinephrine-induced activation of sarcomere reassembly. Recombinant murine MYLK3 shows specificity for Myl2 (Mlc2v) and the phosphorylation is calcium- and calmodulin-dependent.
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