Abstract
Cardiac myosin binding protein-C (MyBP-C) accounts for about half of hypertrophic cardiomyopathy (HCM) mutations, and in the events where another sarcomeric protein is mutated, MyBP-C phosphorylation is frequently altered. MyBP-C is thought to regulate normal cardiac contractility through its interactions with actin and myosin, and this regulation is dependent on phosphorylation. Efforts in elucidating the details of MyBP-C interactions with myosin and actin have been limited due to low-throughput and labor-intensive assays.
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