PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor): defective regulation in failing hearts
Article Abstract:
Regulation by protein kinase A (PKA) of phosphorylation binding of FKBP12.6 to the calcium release channel (ryanodine receptor) is discussed relative to defective regulation in human hearts in decline. RyR2 is PKA hyperphosphorylated and that brings defective channel function caused by increased sensitivity to Ca(super.2+)-induced activation.
author: Marx, Steven O., Reiken, Steven, Hisamatsu, Yuji, Jayaraman, Jayaraman, Burkhoff, Daniel, Rosemblit, Nora, Marks, Andrew R.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2000
Carrier proteins, Transport proteins, Cytochemistry, Protein kinases, Molecular genetics, Sarcoplasmic reticulum
FKBP12.6 deficiency and defective calcium release channel (ryanodine receptor) function linked to exercise-induced sudden cardiac death
Article Abstract:
Research has been conducted on the common cause of sudden cardiac death, arrhythmias. The authors suggest that ryanodine receptor channels can trigger fatal cardial arrhythmias explaining catecholaminergic polymorphic venticular tachycardia.
author: Rosemblit, Nora, Marks, Andrew R., Priori, Silvia G., Napolitano, Carlo, Song, Long-Sheng, Wehrens, Xander H. T., Lehnart, Stephan E., Huang, Fannie, Vest, John A., Reiken, Steven R., Mohler, Peter J., Sun, Jie, Guatimosim, Silvia, D'Armiento, Jeanine M., Memmi, Mirella, Lederer, W. J.
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2003
Italy, Analysis, Causes of, Genetic aspects, Genetic polymorphisms, Cell research, Cytological research, Cardiac arrest, Ventricular tachycardia, Catecholamines, Binding proteins, Sudden cardiac death
Phosphodiesterase 4D deficiency in the ryanodine-receptor complex promotes heart failure and arrhythmias
Article Abstract:
Phosphodiesterases (PDEs) regulate the local concentration of 3',5' cyclic adenosine monophosphate (cAMP) within cells. It is shown that PDE4D gene inactivation in mice results in a progressive cardiomyopathy, accelerated heart failure after myocardial infarction and cardiac arrhythmias.
author: Reiken, Steven, Marks, Andrew R., Lehnart, Stephan E., Wehrens, Xander H.T., Warrier, Sunita, Belevych, Andriy E., Harvey, Robert D., Richter, Wito, Jin, Catherine S.L., Conti, Marco
Publisher: Elsevier B.V.
Publication Name: Cell
Subject: Biological sciences
ISSN: 0092-8674
Year: 2005
Science & research, Risk factors, Heart failure, Cyclic adenylic acid, Cyclic adenosine monophosphate, Phosphodiesterases
subjects list: Research, United States, Physiological aspects, Calcium channels, Heart muscle, Myocardium, Arrhythmia
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