Increased myofilament Ca(2+) sensitivity and diastolic dysfunction as early consequences of Mybpc3 mutation in heterozygous knock-in mice

Lignende værker

• Novel Role for p90 Ribosomal S6 Kinase in the Regulation of Cardiac Myofilament Phosphorylation
  af: Cuello, Friederike, et al.
  Udgivet: (2011)
• Diltiazem prevents stress‐induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3‐knock‐in mice
  af: Flenner, Frederik, et al.
  Udgivet: (2017)
• Distinct Sarcomeric Substrates Are Responsible for Protein Kinase D-mediated Regulation of Cardiac Myofilament Ca(2+) Sensitivity and Cross-bridge Cycling
  af: Bardswell, Sonya C., et al.
  Udgivet: (2010)
• Epigallocatechin-3-Gallate Accelerates Relaxation and Ca(2+) Transient Decay and Desensitizes Myofilaments in Healthy and Mybpc3-Targeted Knock-in Cardiomyopathic Mice
  af: Friedrich, Felix W., et al.
  Udgivet: (2016)
• Rescue of cardiomyopathy through U7snRNA-mediated exon skipping in Mybpc3-targeted knock-in mice
  af: Gedicke-Hornung, Christina, et al.
  Udgivet: (2013)