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Tail Length and E525K Dilated Cardiomyopathy Mutant Alter Human β-Cardiac Myosin Super-Relaxed State.

Sebastian Duno-MirandaShane R NelsonDavid V RasicciSkylar L M BodtJoseph A CiriloDuha VangSivaraj SivaramakrishnanChristopher M YengoDavid M Warshaw
Published in: bioRxiv : the preprint server for biology (2023)
This research investigates the E525K mutation in human β-cardiac myosin, crucial for heart contraction, and its role in causing Dilated Cardiomyopathy (DCM). It demonstrates that the length of the myosin tail influences its self-inhibition, and the E525K mutation strengthens this effect, potentially reducing heart contractility in DCM.
Keyphrases
  • endothelial cells
  • binding protein
  • heart failure
  • induced pluripotent stem cells
  • pluripotent stem cells
  • atrial fibrillation
  • smooth muscle