D
Donald M. Bers
Researcher at University of California, Davis
Publications - 607
Citations - 57349
Donald M. Bers is an academic researcher from University of California, Davis. The author has contributed to research in topics: Ryanodine receptor & Ca2+/calmodulin-dependent protein kinase. The author has an hindex of 118, co-authored 570 publications receiving 52757 citations. Previous affiliations of Donald M. Bers include University of Maryland, Baltimore & Loyola University Medical Center.
Papers
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Journal ArticleDOI
Screening drug-induced arrhythmia events using human induced pluripotent stem cell-derived cardiomyocytes and low-impedance microelectrode arrays
Enrique G. Navarrete,Ping Liang,Feng Lan,Veronica Sanchez-Freire,Chelsey S. Simmons,Tingyu Gong,Arun Sharma,Paul W. Burridge,Bhagat Patlolla,Andrew S. Lee,Haodi Wu,Ramin E. Beygui,Sean M. Wu,Robert C. Robbins,Donald M. Bers,Joseph C. Wu +15 more
TL;DR: The data indicate that the MEA/hiPSC-CM assay is a sensitive, robust, and efficient platform for testing drug effectiveness and for arrhythmia screening and may provide significant advantages over current industry standard assays that use immortalized cell lines or animal models.
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Ryanodine receptor phosphorylation by calcium/calmodulin-dependent protein kinase II promotes life-threatening ventricular arrhythmias in mice with heart failure
Ralph J. van Oort,Mark McCauley,Sayali S. Dixit,Laetitia Pereira,Yi Yang,Jonathan L. Respress,Qiongling Wang,Angela C. De Almeida,Darlene G. Skapura,Mark E. Anderson,Donald M. Bers,Xander H.T. Wehrens +11 more
TL;DR: This article showed that increased RyR2 phosphorylation by Ca2+/calmodulin-dependent protein kinase II is both necessary and sufficient to promote lethal ventricular arrhythmias.
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Protein Kinase A Phosphorylation of the Ryanodine Receptor Does Not Affect Calcium Sparks in Mouse Ventricular Myocytes
TL;DR: It is concluded that the PKA-dependent increase in myocyte CaSpF and size is entirely attributable to PLB phosphorylation and consequent enhanced SR Ca2+ load.
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Reactive Oxygen Species–Activated Ca/Calmodulin Kinase IIδ Is Required for Late INa Augmentation Leading to Cellular Na and Ca Overload
Stefan Wagner,Hanna M. Ruff,Sarah L. Weber,Sarah Bellmann,Thomas Sowa,Timo Schulte,Mark E. Anderson,Eleonora Grandi,Donald M. Bers,Johannes Backs,Luiz Belardinelli,Lars S. Maier +11 more
TL;DR: Free [Ca]i and a functional SR are required for ROS activation of CaMKII and this may be of relevance in hear failure, where enhanced ROS production meets increased Ca MKII expression.
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Phosphorylation of phospholamban and troponin I in β-adrenergic-induced acceleration of cardiac relaxation
TL;DR: The effect of beta-adrenergic activation on relaxation is mediated entirely by PLB phosphorylation in the absence of external load, however, TnI phosphorylated could contribute up to 14-18% of this lusitropic effect in the WT mouse during maximal isometric contractions.