Mutations in the gene encoding the sarcomeric protein cardiac myosin-binding protein C (cMyBP-C) are a leading cause of hypertrophic cardiomyopathy (HCM). Mouse models targeting cMyBP-C and use of recombinant proteins have been effective in studying its roles in contractile function and disease. Surprisingly， while the N-terminus of cMyBP-C is important to regulate myofilament binding and contains many HCM mutations， an incorrect sequence， lacking the N-terminal 8 amino acids has been used in many studies.
Mutations in the gene encoding the sarcomeric protein cardiac myosin-binding protein C (cMyBP-C) are a leading cause of hypertrophic cardiomyopathy (HCM). Mouse models targeting cMyBP-C and use of recombinant proteins have been effective in studying its roles in contractile function and disease. Surprisingly， while the N-terminus of cMyBP-C is important to regulate myofilament binding and contains many HCM mutations， an incorrect sequence， lacking the N-terminal 8 amino acids has been used in many studies.
