In the RyR2R4496C Mouse Model of CPVT, &bgr;-Adrenergic Stimulation Induces Ca Waves by Increasing SR Ca Content and Not by Decreasing the Threshold for Ca Waves
暂无分享,去创建一个
Andrew W. Trafford | Carlo Napolitano | Silvia G. Priori | David A. Eisner | S. Priori | C. Napolitano | A. Trafford | D. Eisner | Takeshi Kashimura | Sarah J. Briston | Luigi A. Venetucci | T. Kashimura | L. Venetucci | S. Briston
[1] Heping Cheng,et al. RyR 2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca 2 release ( SOICR ) , 2004 .
[2] A. Trafford,et al. Regulation of systolic [Ca2+]i and cellular Ca2+ flux balance in rat ventricular myocytes by SR Ca2+, L‐type Ca2+ current and diastolic [Ca2+]i , 2007, The Journal of physiology.
[3] D. Roden,et al. Flecainide prevents catecholaminergic polymorphic ventricular tachycardia in mice and humans , 2009, Nature Medicine.
[4] Kenneth R. Laurita,et al. Transmural Heterogeneity of Calcium Handling in Canine , 2003, Circulation research.
[5] P. Coumel,et al. Catecholaminergic polymorphic ventricular tachycardia in children. A 7-year follow-up of 21 patients. , 1995, Circulation.
[6] D. Allen,et al. The effects of 2,3-butanedione monoxime on initial heat, tension, and aequorin light output of ferret papillary muscles , 1990, Pflügers Archiv.
[7] A. Trafford,et al. 2,3-Butanedione monoxime (BDM) decreases sarcoplasmic reticulum Ca content by stimulating Ca release in isolated rat ventricular myocytes , 1998, Pflügers Archiv.
[8] M. Diaz,et al. Enhanced Ca2+ current and decreased Ca2+ efflux restore sarcoplasmic reticulum Ca2+ content after depletion. , 1997, Circulation research.
[9] Guy Vassort,et al. Protein Kinase A Phosphorylation of the Cardiac Calcium Release Channel (Ryanodine Receptor) in Normal and Failing Hearts , 2003, The Journal of Biological Chemistry.
[10] Johnson Francis,et al. Catecholaminergic polymorphic ventricular tachycardia. , 2005, Heart rhythm.
[11] M. Diaz,et al. Modulation of CICR has no maintained effect on systolic Ca2+: simultaneous measurements of sarcoplasmic reticulum and sarcolemmal Ca2+ fluxes in rat ventricular myocytes , 2000, The Journal of physiology.
[12] R. Hinch,et al. Interplay between SERCA and sarcolemmal Ca2+ efflux pathways controls spontaneous release of Ca2+ from the sarcoplasmic reticulum in rat ventricular myocytes , 2004, The Journal of physiology.
[13] M. Yano,et al. Catecholaminergic Polymorphic Ventricular Tachycardia Is Caused by Mutation-Linked Defective Conformational Regulation of the Ryanodine Receptor , 2010, Circulation research.
[14] A. Trafford,et al. Increasing Ryanodine Receptor Open Probability Alone Does Not Produce Arrhythmogenic Calcium Waves: Threshold Sarcoplasmic Reticulum Calcium Content Is Required , 2007, Circulation research.
[15] M. Rosen,et al. Mechanisms of Digitalis Toxicity: Effects of Ouabain on Phase Four of Canine Purkinje Fiber Transmembrane Potentials , 1973, Circulation.
[16] M. Varsányi,et al. Phosphorylation of skeletal muscle calsequestrin enhances its Ca2+ binding capacity and promotes its association with junctin. , 2008, Cell calcium.
[17] S. Priori,et al. Increased Ca 2 (cid:1) Sensitivity of the Ryanodine Receptor Mutant RyR2 R4496C Underlies Catecholaminergic Polymorphic Ventricular Tachycardia , 2008 .
[18] A. Trafford,et al. The sarcoplasmic reticulum and arrhythmogenic calcium release. , 2008, Cardiovascular research.
[19] A. Varró,et al. An estimate of the calcium content of the sarcoplasmic reticulum in rat ventricular myocytes , 1993, Pflügers Archiv.
[20] R. Nagai,et al. The mechanism of catecholaminergic polymorphic ventricular tachycardia may be triggered activity due to delayed afterdepolarization. , 1997, European heart journal.
[21] K. Dilly,et al. Mechanisms underlying variations in excitation–contraction coupling across the mouse left ventricular free wall , 2006, The Journal of physiology.
[22] Huihui Kong,et al. Enhanced Store Overload–Induced Ca2+ Release and Channel Sensitivity to Luminal Ca2+ Activation Are Common Defects of RyR2 Mutations Linked to Ventricular Tachycardia and Sudden Death , 2005, Circulation research.
[23] A. Trafford,et al. What role does modulation of the ryanodine receptor play in cardiac inotropy and arrhythmogenesis? , 2009, Journal of molecular and cellular cardiology.
[24] D. Burkhoff,et al. PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor) Defective Regulation in Failing Hearts , 2000, Cell.
[25] K. Brown,et al. Mutations of the Cardiac Ryanodine Receptor (RyR2) Gene in Familial Polymorphic Ventricular Tachycardia , 2001, Circulation.
[26] Heping Cheng,et al. RyR2 mutations linked to ventricular tachycardia and sudden death reduce the threshold for store-overload-induced Ca2+ release (SOICR). , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[27] Wenjun Xie,et al. Functional Consequence of Protein Kinase A-dependent Phosphorylation of the Cardiac Ryanodine Receptor , 2007, Journal of Biological Chemistry.
[28] S. Priori,et al. Arrhythmogenesis in Catecholaminergic Polymorphic Ventricular Tachycardia: Insights From a RyR2 R4496C Knock-In Mouse Model , 2006 .
[29] G. Ferrier,et al. A Cellular Mechanism for the Generation of Ventricular Arrhythmias by Acetylstrophanthidin , 1973, Circulation research.
[30] Wei Zhang,et al. Mice with the R176Q cardiac ryanodine receptor mutation exhibit catecholamine-induced ventricular tachycardia and cardiomyopathy , 2006, Proceedings of the National Academy of Sciences.
[31] M. Diaz,et al. Measurement of sarcoplasmic reticulum Ca2+ content and sarcolemmal Ca2+ fluxes in isolated rat ventricular myocytes during spontaneous Ca2+ release , 1997, The Journal of physiology.
[32] Godfrey L. Smith,et al. The effects of metabolic inhibition on intracellular calcium and pH in isolated rat ventricular cells. , 1989, The Journal of physiology.
[33] W. Lederer,et al. Modulation of cardiac ryanodine receptors of swine and rabbit by a phosphorylation‐dephosphorylation mechanism. , 1995, The Journal of physiology.
[34] Carlo Napolitano,et al. Increased Ca2+ Sensitivity of the Ryanodine Receptor Mutant RyR2R4496C Underlies Catecholaminergic Polymorphic Ventricular Tachycardia , 2009, Circulation research.
[35] G. R. Fitzgerald,et al. Bidirectional tachycardia in a child. A study using His bundle electrography. , 1975, British heart journal.
[36] C. Antzelevitch,et al. Transmural heterogeneity of calcium activity and mechanical function in the canine left ventricle. , 2004, American journal of physiology. Heart and circulatory physiology.
[37] M. Diaz,et al. Reducing Ryanodine Receptor Open Probability as a Means to Abolish Spontaneous Ca2+ Release and Increase Ca2+ Transient Amplitude in Adult Ventricular Myocytes , 2006, Circulation research.
[38] S. Priori,et al. FKBP12.6 Deficiency and Defective Calcium Release Channel (Ryanodine Receptor) Function Linked to Exercise-Induced Sudden Cardiac Death , 2003, Cell.
[39] 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 .
[40] S. Priori,et al. Mutations in the Cardiac Ryanodine Receptor Gene (hRyR2) Underlie Catecholaminergic Polymorphic Ventricular Tachycardia , 2001, Circulation.
[41] José Jalife,et al. Arrhythmogenic Mechanisms in a Mouse Model of Catecholaminergic Polymorphic Ventricular Tachycardia , 2007, Circulation research.
[42] M. Viitasalo,et al. Clinical Research , 2022 .
[43] M. Diaz,et al. A measurable reduction of s.r. Ca content follows spontaneous Ca release in rat ventricular myocytes , 1997, Pflügers Archiv.
[44] D. Bers,et al. Quantitative Assessment of the SR Ca2+ Leak-Load Relationship , 2002, Circulation research.
[45] S. Priori,et al. Na+-dependent SR Ca2+ overload induces arrhythmogenic events in mouse cardiomyocytes with a human CPVT mutation. , 2010, Cardiovascular research.
[46] A. Katz,et al. The stimulation of calcium transport in cardiac sarcoplasmic reticulum by adenosine 3':5'-monophosphate-dependent protein kinase. , 1974, The Journal of biological chemistry.