Progression of heart failure: is protein kinase a hyperphosphorylation of the ryanodine receptor a contributing factor?
Marks
Andrew R
AR
Center for Molecular Cardiology, Department of Pharmacology, Columbia University College of Physicians and Surgeons, New York, NY, USA. arm42@columbia.edu
Reiken
Steven
S
Marx
Steven O
SO
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology; D002118:Calcium / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism*; D018450:Disease Progression; D020022:Genetic Predisposition to Disease; D006333:Heart Failure / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D008955:Models, Cardiovascular; D009154:Mutation; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D010766:Phosphorylation; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D015398:Signal Transduction
D000319:Adrenergic beta-Antagonists; D019837:Ryanodine Receptor Calcium Release Channel; D017868:Cyclic AMP-Dependent Protein Kinases; D002118:Calcium