Loss of Protein Phosphatase 1 Regulatory Subunit PPP1R3A Promotes Atrial Fibrillation

BACKGROUND:Abnormal calcium (Ca) release from the sarcoplasmic reticulum (SR) contributes to the pathogenesis of atrial fibrillation (AF). Increased phosphorylation of 2 proteins essential for normal SR-Ca cycling, the type-2 ryanodine receptor (RyR2) and phospholamban (PLN), enhances the susceptibi...

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Veröffentlicht in:	Circulation (New York, N.Y.) N.Y.), 2019-08, Vol.140 (8), p.681-693
Hauptverfasser:	Alsina, Katherina M, Hulsurkar, Mohit, Brandenburg, Sören, Kownatzki-Danger, Daniel, Lenz, Christof, Urlaub, Henning, Abu-Taha, Issam, Kamler, Markus, Chiang, David Y, Lahiri, Satadru K, Reynolds, Julia O, Quick, Ann P, Scott, Larry, Word, Tarah A, Gelves, Maria D, Heck, Albert J.R, Li, Na, Dobrev, Dobromir, Lehnart, Stephan E, Wehrens, Xander H.T
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Atrial Fibrillation - genetics Atrial Fibrillation - metabolism Calcium - metabolism Calcium-Binding Proteins - metabolism Cells, Cultured Disease Models, Animal Disease Susceptibility Humans Mice Mice, Knockout Myocytes, Cardiac - physiology Phosphoprotein Phosphatases - genetics Phosphoprotein Phosphatases - metabolism Protein Phosphatase 1 - metabolism Proteomics Ryanodine Receptor Calcium Release Channel - metabolism Sarcoplasmic Reticulum - metabolism Signal Transduction
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