The Ca2+ leak paradox and “rogue ryanodine receptors”: SR Ca2+ efflux theory and practice

[1]  R. Tsien,et al.  Transient inward current underlying arrhythmogenic effects of cardiotonic steroids in Purkinje fibres. , 1976, The Journal of physiology.

[2]  R Weingart,et al.  Role of calcium ions in transient inward currents and aftercontractions induced by strophanthidin in cardiac Purkinje fibres. , 1978, The Journal of physiology.

[3]  W. Lederer,et al.  Cellular Origins of the Transient Inward Current in Cardiac Myocytes. Role of Fluctuations and Waves of Elevated Intracellular Calcium , 1989, Circulation research.

[4]  Donald M. Bers,et al.  Excitation-Contraction Coupling and Cardiac Contractile Force , 1991, Developments in Cardiovascular Medicine.

[5]  W. Lederer,et al.  Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle. , 1993, Science.

[6]  G. Ellis‐Davies,et al.  Rapid adaptation of cardiac ryanodine receptors: modulation by Mg2+ and phosphorylation. , 1995, Science.

[7]  W. Lederer,et al.  Calcium sparks and [Ca2+]i waves in cardiac myocytes. , 1996, The American journal of physiology.

[8]  W. Lederer,et al.  Defective excitation-contraction coupling in experimental cardiac hypertrophy and heart failure. , 1997, Science.

[9]  F. Protasi,et al.  Comparative Ultrastructure of Ca2+ Release Units in Skeletal and Cardiac Muscle , 1998, Annals of the New York Academy of Sciences.

[10]  J. Changeux,et al.  Allosteric receptors after 30 years , 1998, Neuron.

[11]  T. Duke,et al.  Heightened sensitivity of a lattice of membrane receptors. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[12]  F. Protasi,et al.  Shape, size, and distribution of Ca(2+) release units and couplons in skeletal and cardiac muscles. , 1999, Biophysical journal.

[13]  Michael D. Stern,et al.  Local Control Models of Cardiac Excitation–Contraction Coupling , 1999, The Journal of general physiology.

[14]  M. Yano,et al.  Altered interaction of FKBP12.6 with ryanodine receptor as a cause of abnormal Ca(2+) release in heart failure. , 2000, Cardiovascular research.

[15]  D. Burkhoff,et al.  PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor) Defective Regulation in Failing Hearts , 2000, Cell.

[16]  A. Marks.  Ryanodine receptors/calcium release channels in heart failure and sudden cardiac death. , 2001, Journal of molecular and cellular cardiology.

[17]  Godfrey L. Smith,et al.  Overexpression of FK506-Binding Protein FKBP12.6 in Cardiomyocytes Reduces Ryanodine Receptor–Mediated Ca2+ Leak From the Sarcoplasmic Reticulum and Increases Contractility , 2001, Circulation research.

[18]  M. Diaz,et al.  Coordinated Control of Cell Ca 2 1 Loading and Triggered Release From the Sarcoplasmic Reticulum Underlies the Rapid Inotropic Response to Increased L-Type Ca 2 1 Current , 2001 .

[19]  Li Li,et al.  Arrhythmogenesis and Contractile Dysfunction in Heart Failure: Roles of Sodium-Calcium Exchange, Inward Rectifier Potassium Current, and Residual &bgr;-Adrenergic Responsiveness , 2001, Circulation research.

[20]  S. Marx,et al.  Coupled Gating Between Cardiac Calcium Release Channels (Ryanodine Receptors) , 2001, Circulation research.

[21]  N Le Novère,et al.  Conformational spread in a ring of proteins: a stochastic approach to allostery. , 2001, Journal of molecular biology.

[22]  D. Bers,et al.  Protein Kinase A Phosphorylation of the Ryanodine Receptor Does Not Affect Calcium Sparks in Mouse Ventricular Myocytes , 2002, Circulation research.

[23]  D. Terentyev,et al.  Luminal Ca2+ Controls Termination and Refractory Behavior of Ca2+-Induced Ca2+ Release in Cardiac Myocytes , 2002, Circulation research.

[24]  P. Lipp,et al.  Spatial characteristics of sarcoplasmic reticulum Ca2+ release events triggered by L‐type Ca2+ current and Na+ current in guinea‐pig cardiac myocytes , 2002, The Journal of physiology.

[25]  Mark A. Magnuson,et al.  Oestrogen protects FKBP12.6 null mice from cardiac hypertrophy , 2002, Nature.

[26]  R. Haworth,et al.  Abnormal Ca2+ Release, but Normal Ryanodine Receptors, in Canine and Human Heart Failure , 2002, Circulation research.

[27]  Eric A Sobie,et al.  Termination of cardiac Ca(2+) sparks: an investigative mathematical model of calcium-induced calcium release. , 2002, Biophysical journal.

[28]  S. Priori,et al.  FKBP12.6 Deficiency and Defective Calcium Release Channel (Ryanodine Receptor) Function Linked to Exercise-Induced Sudden Cardiac Death , 2003, Cell.

[29]  E. Ríos,et al.  Unitary Ca2+ Current through Mammalian Cardiac and Amphibian Skeletal Muscle Ryanodine Receptor Channels under Near-physiological Ionic Conditions , 2003, The Journal of general physiology.

[30]  Donald M Bers,et al.  Sarcoplasmic reticulum Ca2+ and heart failure: roles of diastolic leak and Ca2+ transport. , 2003, Circulation research.

[31]  Gustavo Stolovitzky,et al.  Ising model of cardiac thin filament activation with nearest-neighbor cooperative interactions. , 2003, Biophysical journal.

[32]  A. Marks.  A guide for the perplexed: towards an understanding of the molecular basis of heart failure. , 2003, Circulation.

[33]  D. Bers,et al.  Elevated Sarcoplasmic Reticulum Ca2+ Leak in Intact Ventricular Myocytes From Rabbits in Heart Failure , 2003, Circulation research.

[34]  J. Ross,et al.  Calcium and heart failure: the cycle game , 2003, Nature Medicine.

[35]  M. Diaz,et al.  Sarcoplasmic Reticulum Calcium Content Fluctuation Is the Key to Cardiac Alternans , 2004, Circulation research.

[36]  D. Heisey,et al.  Ca transients from Ca channel activity in rat cardiac myocytes reveal dynamics of dyad cleft and troponin C Ca binding. , 2004, American journal of physiology. Cell physiology.

[37]  T. Duke,et al.  Conformational spread: the propagation of allosteric states in large multiprotein complexes. , 2004, Annual review of biophysics and biomolecular structure.

[38]  P. Brookes,et al.  Calcium, ATP, and ROS: a mitochondrial love-hate triangle. , 2004, American journal of physiology. Cell physiology.

[39]  E. McNally,et al.  Nesprin-1alpha contributes to the targeting of mAKAP to the cardiac myocyte nuclear envelope. , 2005, Experimental cell research.

[40]  E. Niggli,et al.  Paradoxical SR Ca2+ release in guinea‐pig cardiac myocytes after β‐adrenergic stimulation revealed by two‐photon photolysis of caged Ca2+ , 2005, The Journal of physiology.