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  1. Molecular basis of force-pCa relation in MYL2 cardiomyopathy mice: Role of the super-relaxed state of myosin
  2. Slow-twitch skeletal muscle defects accompany cardiac dysfunction in transgenic mice with a mutation in the myosin regulatory light chain
  3. Cardiac contractility, motor function, and cross‐bridge kinetics in N47K‐ RLC mutant mice
  4. Hypercontractile mutant of ventricular myosin essential light chain leads to disruption of sarcomeric structure and function and results in restrictive cardiomyopathy in mice
  5. Myosin light chain phosphorylation, novel targets to repair a broken heart?
  6. Novel familial dilated cardiomyopathy mutation inMYL2affects the structure and function of myosin regulatory light chain
  7. The effect of myosin RLC phosphorylation in normal and cardiomyopathic mouse hearts
  8. Myosin motors abnormalities lead to dilated cardiomyopathy