Post-translational control of cardiac hemodynamics through myosin binding protein C

Pflugers Arch. 2014 Feb;466(2):231-6. doi: 10.1007/s00424-013-1377-y. Epub 2013 Oct 22.

Abstract

Cardiac myosin binding protein C (cMyBP-C) is an integral sarcomeric protein that associates with the thick, thin, and titin filament systems in the contractile apparatus. Three different isoforms of MyBP-C exist in mammalian muscle: slow skeletal (MyBPC1), fast skeletal (MyBP-C2, with several variants), and cardiac (cMyBP-C). Genetic screening studies show that mutations in MYBPC3 occur frequently and are responsible for as many as 30-35 % of identified cases of familial hypertrophic cardiomyopathy. The function of cMyBP-C is stringently regulated by its post-translational modification. In particular, the addition of phosphate groups occurs with high frequency on certain serine residues that are located in the cardiac-specific regulatory M domain. Phosphorylation of this domain has been extensively studied in vitro and in vivo. Phosphorylation of the M domain can regulate the manner in which actin and myosin interact, affecting the cross bridge cycle and ultimately, cardiac hemodynamics.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Actins / metabolism
  • Animals
  • Carrier Proteins / metabolism*
  • Cyclic AMP-Dependent Protein Kinases / metabolism
  • Hemodynamics
  • Humans
  • Myocardial Contraction / physiology*
  • Myocardium / metabolism
  • Myofibrils / metabolism
  • Myosins / metabolism
  • Phosphorylation
  • Protein Processing, Post-Translational
  • Sarcomeres / metabolism

Substances

  • Actins
  • Carrier Proteins
  • myosin-binding protein C
  • Cyclic AMP-Dependent Protein Kinases
  • Myosins