Sandor Gyorke

Summary

Affiliation: The Ohio State University
Country: USA

Publications

  1. ncbi request reprint Genetic ablation of ryanodine receptor 2 phosphorylation at Ser-2808 aggravates Ca2+-dependent cardiomyopathy by exacerbating diastolic Ca2+ release
    Bin Liu
    Department of Physiology and Cell Biology, 507 Davis Heart and Lung Research Institute office, 473 W 12th Avenue, Columbus, OH 43210, USA
    J Physiol 592:1957-73. 2014
  2. ncbi request reprint Modulation of ryanodine receptor by luminal calcium and accessory proteins in health and cardiac disease
    Sandor Gyorke
    Department of Physiology and Cell Biology, 505 Davis Heart and Lung Research Institute, The Ohio State University, 473 West 12th Avenue, Columbus, OH 43210, USA
    Cardiovasc Res 77:245-55. 2008
  3. doi request reprint Molecular basis of catecholaminergic polymorphic ventricular tachycardia
    Sandor Gyorke
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio 43210, USA
    Heart Rhythm 6:123-9. 2009
  4. pmc Dysregulated sarcoplasmic reticulum calcium release: potential pharmacological target in cardiac disease
    Sandor Gyorke
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States
    Pharmacol Ther 119:340-54. 2008
  5. pmc Shortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death
    Andriy E Belevych
    Davis Heart and Lung Research Institute, The Ohio State University Medical Center, 473 W 12th Ave, Columbus, OH 43210, USA
    Circ Res 110:569-77. 2012
  6. pmc Redox modification of ryanodine receptors underlies calcium alternans in a canine model of sudden cardiac death
    Andriy E Belevych
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University, College of Medicine, Columbus, OH 43210, USA
    Cardiovasc Res 84:387-95. 2009
  7. pmc Chronic heart failure and the substrate for atrial fibrillation
    Arun Sridhar
    Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA
    Cardiovasc Res 84:227-36. 2009
  8. pmc Abnormal intrastore calcium signaling in chronic heart failure
    Zuzana Kubalova
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, Ohio State University, Columbus, OH 43210, USA
    Proc Natl Acad Sci U S A 102:14104-9. 2005
  9. pmc Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death
    Ingrid M Bonilla
    College of Pharmacy, The Ohio State University, Columbus, Ohio 43210, USA
    J Appl Physiol (1985) 113:1772-83. 2012
  10. pmc Functional consequences of stably expressing a mutant calsequestrin (CASQ2D307H) in the CASQ2 null background
    Anuradha Kalyanasundaram
    Department of Physiology and Cell Biology, The Ohio State University College of Medicine, Columbus, USA
    Am J Physiol Heart Circ Physiol 302:H253-61. 2012

Collaborators

Detail Information

Publications49

  1. ncbi request reprint Genetic ablation of ryanodine receptor 2 phosphorylation at Ser-2808 aggravates Ca2+-dependent cardiomyopathy by exacerbating diastolic Ca2+ release
    Bin Liu
    Department of Physiology and Cell Biology, 507 Davis Heart and Lung Research Institute office, 473 W 12th Avenue, Columbus, OH 43210, USA
    J Physiol 592:1957-73. 2014
    ....
  2. ncbi request reprint Modulation of ryanodine receptor by luminal calcium and accessory proteins in health and cardiac disease
    Sandor Gyorke
    Department of Physiology and Cell Biology, 505 Davis Heart and Lung Research Institute, The Ohio State University, 473 West 12th Avenue, Columbus, OH 43210, USA
    Cardiovasc Res 77:245-55. 2008
    ..Acquired and genetic defects in proteins of this junctional Ca(2+) signalling complex lead to disease states such as cardiac arrhythmia and heart failure by impairing luminal Ca(2+) regulation of RyR2...
  3. doi request reprint Molecular basis of catecholaminergic polymorphic ventricular tachycardia
    Sandor Gyorke
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, Ohio 43210, USA
    Heart Rhythm 6:123-9. 2009
    ..Similar mechanisms may apply to arrhythmias during various conditions, including heart failure and ischemic heart disease, associated with acquired defects in components of the Ca(2+) release channel complex...
  4. pmc Dysregulated sarcoplasmic reticulum calcium release: potential pharmacological target in cardiac disease
    Sandor Gyorke
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, United States
    Pharmacol Ther 119:340-54. 2008
    ..We will also discuss the relationships between abnormal SR Ca(2+) release and various cardiac disease phenotypes, including, arrhythmias and heart failure, and consider SR Ca(2+) release as a potential therapeutic target...
  5. pmc Shortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death
    Andriy E Belevych
    Davis Heart and Lung Research Institute, The Ohio State University Medical Center, 473 W 12th Ave, Columbus, OH 43210, USA
    Circ Res 110:569-77. 2012
    ....
  6. pmc Redox modification of ryanodine receptors underlies calcium alternans in a canine model of sudden cardiac death
    Andriy E Belevych
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University, College of Medicine, Columbus, OH 43210, USA
    Cardiovasc Res 84:387-95. 2009
    ....
  7. pmc Chronic heart failure and the substrate for atrial fibrillation
    Arun Sridhar
    Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA
    Cardiovasc Res 84:227-36. 2009
    ..We sought to define the underlying mechanisms for atrial fibrillation (AF) during chronic heart failure (HF)...
  8. pmc Abnormal intrastore calcium signaling in chronic heart failure
    Zuzana Kubalova
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, Ohio State University, Columbus, OH 43210, USA
    Proc Natl Acad Sci U S A 102:14104-9. 2005
    ..This work shows that the diminished SR Ca release characteristic of failing myocardium could be explained by increased sensitivity of RyRs to luminal Ca, leading to enhanced spark-mediated SR Ca leak and reduced intra-SR [Ca]...
  9. pmc Endurance exercise training normalizes repolarization and calcium-handling abnormalities, preventing ventricular fibrillation in a model of sudden cardiac death
    Ingrid M Bonilla
    College of Pharmacy, The Ohio State University, Columbus, Ohio 43210, USA
    J Appl Physiol (1985) 113:1772-83. 2012
    ..05). Exercise training prevented ischemically induced VF, in association with a combination of beneficial effects on cellular electrophysiology and calcium handling...
  10. pmc Functional consequences of stably expressing a mutant calsequestrin (CASQ2D307H) in the CASQ2 null background
    Anuradha Kalyanasundaram
    Department of Physiology and Cell Biology, The Ohio State University College of Medicine, Columbus, USA
    Am J Physiol Heart Circ Physiol 302:H253-61. 2012
    ..We propose that poor interaction between CASQ2(D307H) and triadin 1 could affect ryanodine receptor 2 stability, thereby increasing susceptibility to delayed afterdepolarizations and triggered arrhythmic activity...
  11. pmc MicroRNA-1 and -133 increase arrhythmogenesis in heart failure by dissociating phosphatase activity from RyR2 complex
    Andriy E Belevych
    The Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America
    PLoS ONE 6:e28324. 2011
    ....
  12. pmc Protein protein interactions between triadin and calsequestrin are involved in modulation of sarcoplasmic reticulum calcium release in cardiac myocytes
    Dmitry Terentyev
    Department of Physiology and Cell Biology, 505 Davis Heart and Lung Research Institute, The Ohio State University, 473 W 12th Ave, Columbus, OH 43210, USA
    J Physiol 583:71-80. 2007
    ....
  13. ncbi request reprint miR-1 overexpression enhances Ca(2+) release and promotes cardiac arrhythmogenesis by targeting PP2A regulatory subunit B56alpha and causing CaMKII-dependent hyperphosphorylation of RyR2
    Dmitry Terentyev
    Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, Ohio State University, Columbus, OH 43210, USA
    Circ Res 104:514-21. 2009
    ..We conclude that miR-1 enhances cardiac excitation-contraction coupling by selectively increasing phosphorylation of the L-type and RyR2 channels via disrupting localization of PP2A activity to these channels...
  14. pmc Decreased RyR2 refractoriness determines myocardial synchronization of aberrant Ca2+ release in a genetic model of arrhythmia
    Lucia Brunello
    D Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
    Proc Natl Acad Sci U S A 110:10312-7. 2013
    ..Our study reveals how aberrant DCR events can become synchronized in the intact myocardium, leading to triggered activity and the resultant DCs in the settings of a cardiac rhythm disorder...
  15. pmc Modulation of SR Ca release by luminal Ca and calsequestrin in cardiac myocytes: effects of CASQ2 mutations linked to sudden cardiac death
    Dmitry Terentyev
    Department of Physiology, Dorothy M Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, Ohio 43210 1252, USA
    Biophys J 95:2037-48. 2008
    ..Furthermore, two CPVT-inducing CASQ2 mutations, which cause mechanistically different defects in CASQ2 and RyR2 function, lead to increased diastolic SR Ca release events and exhibit a similar CPVT disease phenotype...
  16. pmc The relationship between arrhythmogenesis and impaired contractility in heart failure: role of altered ryanodine receptor function
    Andriy E Belevych
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Medical Center, 473 W 12th Avenue Columbus, OH 43210, USA
    Cardiovasc Res 90:493-502. 2011
    ..In the present study, we investigated the relationships between Ca(2+) handling, reduced myocyte contractility, and enhanced arrhythmogenesis during HF progression in a canine model of non-ischaemic HF...
  17. pmc Intra-sarcoplasmic reticulum Ca2+ oscillations are driven by dynamic regulation of ryanodine receptor function by luminal Ca2+ in cardiomyocytes
    Sarah C W Stevens
    Department of Physiology and Cell Biology, Ohio State University, Columbus, OH 43214, USA
    J Physiol 587:4863-72. 2009
    ..Deactivation at reduced [Ca(2+)]SR appears to involve reduction of sensitivity to cytosolic Ca(2+) and might be mediated by CASQ2. Inactivation by cytosolic Ca(2+) plays no detectable role in controlling SR Ca(2+) release...
  18. pmc Effects of dietary omega-3 fatty acids on ventricular function in dogs with healed myocardial infarctions: in vivo and in vitro studies
    George E Billman
    Dept of Physiology and Cell Biology, The Ohio State Univ, Columbus, 43210 1218, USA
    Am J Physiol Heart Circ Physiol 298:H1219-28. 2010
    ..Thus dietary n-3 PUFAs did not adversely alter either in vitro or in vivo ventricular contractile function in dogs with healed infarctions...
  19. pmc Arrhythmogenic adverse effects of cardiac glycosides are mediated by redox modification of ryanodine receptors
    Hsiang Ting Ho
    Davis Heart and Lung Research Institute, The Ohio State University Medical Centre, 473 W 12th Avenue, Columbus, OH 43210, USA
    J Physiol 589:4697-708. 2011
    ..These CG-dependent effects probably involve release of ROS from mitochondria possibly mediated by NADPH oxidase...
  20. pmc Repolarization abnormalities and afterdepolarizations in a canine model of sudden cardiac death
    Arun Sridhar
    Davis Heart and Lung Research Institute, Ohio State University, Columbus, Ohio 43210, USA
    Am J Physiol Regul Integr Comp Physiol 295:R1463-72. 2008
    ..These abnormalities may provide a substrate for initiation of postmyocardial infarction ventricular tachyarrhythmias...
  21. pmc Tetrahydrobiopterin depletion and NOS2 uncoupling contribute to heart failure-induced alterations in atrial electrophysiology
    Yoshinori Nishijima
    College of Pharmacy, The Ohio State University, 500 W 12th Avenue, Columbus, OH 43210, USA
    Cardiovasc Res 91:71-9. 2011
    ..Chronic canine heart failure reduces atrial action potential duration and atrial refractoriness. We hypothesized that inducible nitric oxide synthase 2 (NOS2) contributes to atrial oxidative stress and electrophysiologic alterations...
  22. pmc Calsequestrin determines the functional size and stability of cardiac intracellular calcium stores: Mechanism for hereditary arrhythmia
    Dmitry Terentyev
    Department of Physiology and Cell Biology, Texas Tech University Health Sciences Center, Lubbock, TX 79430 6551, USA
    Proc Natl Acad Sci U S A 100:11759-64. 2003
    ..The abnormal restitution of Ca-release channels in the presence of reduced CSQ2 levels provides a plausible explanation for ventricular arrhythmia associated with mutations of CSQ2...
  23. doi request reprint Probing cationic selectivity of cardiac calsequestrin and its CPVT mutants
    Naresh C Bal
    Department of Physiology and Cell Biology, The Ohio State University College of Medicine, Columbus, OH 43210, USA
    Biochem J 435:391-9. 2011
    ..In conclusion, these studies suggest that CPVT mutations modify CASQ2 behaviour, including folding, aggregation/polymerization and selectivity towards Ca2+...
  24. pmc Enhanced ryanodine receptor-mediated calcium leak determines reduced sarcoplasmic reticulum calcium content in chronic canine heart failure
    Andriy Belevych
    Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, Ohio State University Medical Center, Columbus, Ohio 43210, USA
    Biophys J 93:4083-92. 2007
    ..Taken together, these results suggest that RyR2-mediated SR Ca(2+) leak is a major factor in the abnormal intracellular Ca(2+) handling that critically contributes to the reduced SR Ca(2+) content of failing cardiomyocytes...
  25. ncbi request reprint Abnormal interactions of calsequestrin with the ryanodine receptor calcium release channel complex linked to exercise-induced sudden cardiac death
    Dmitry Terentyev
    Department of Physiology and Cell Biology, Heart and Lung Research Institute, Ohio State University, Columbus, OH 43210, USA
    Circ Res 98:1151-8. 2006
    ..These results show that intracellular Ca2+ cycling in normal heart relies on an intricate interplay of CASQ2 with the proteins of the RyR2 channel complex and that disruption of these interactions can lead to cardiac arrhythmia...
  26. pmc Neuronal nitric oxide synthase is indispensable for the cardiac adaptive effects of exercise
    Steve R Roof
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA
    Basic Res Cardiol 108:332. 2013
    ..This pathway may provide a potential novel therapeutic target in cardiac patients who are unable or unwilling to exercise...
  27. pmc Redox modification of ryanodine receptors contributes to sarcoplasmic reticulum Ca2+ leak in chronic heart failure
    Dmitry Terentyev
    Departments of Physiology and Cell Biology, College of Medicine, Ohio State University, Columbus, OH, USA
    Circ Res 103:1466-72. 2008
    ..These findings suggest that redox modification contributes to abnormal function of RyR2s in HF, presenting a potential therapeutic target for treating HF...
  28. ncbi request reprint Triadin overexpression stimulates excitation-contraction coupling and increases predisposition to cellular arrhythmia in cardiac myocytes
    Dmitry Terentyev
    Department of Physiology and Cell Biology, Heart and Lung Research Institute, Ohio State University, Columbus, Ohio 43210, USA
    Circ Res 96:651-8. 2005
    ..We conclude that TRD enhances cardiac excitation-contraction coupling by directly stimulating the RyR2. Interaction of TRD with RyR2 may involve amino acids 200 to 224 in C-terminal domain of TRD...
  29. pmc Store-dependent deactivation: cooling the chain-reaction of myocardial calcium signaling
    Przemysław B Radwański
    The Dorothy M Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA
    J Mol Cell Cardiol 58:77-83. 2013
    ....
  30. pmc Diesterified nitrone rescues nitroso-redox levels and increases myocyte contraction via increased SR Ca(2+) handling
    Christopher J Traynham
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA
    PLoS ONE 7:e52005. 2012
    ..The concurrent restoration of NO and O(2) (.-) levels may have therapeutic potential in the treatment of various cardiomyopathies...
  31. pmc Mechanisms of impaired calcium handling underlying subclinical diastolic dysfunction in diabetes
    Veronique A Lacombe
    College of Pharmacy, The Ohio State University, Columbus, OH 43210, USA
    Am J Physiol Regul Integr Comp Physiol 293:R1787-97. 2007
    ..These data suggest that in vitro impairment of Ca(2+) reuptake during myocyte relaxation contributes to in vivo diastolic dysfunction, with preserved global systolic function, during diabetes...
  32. pmc A mutation in calsequestrin, CASQ2D307H, impairs Sarcoplasmic Reticulum Ca2+ handling and causes complex ventricular arrhythmias in mice
    Wessel P Dirksen
    Department of Physiology and Cell Biology, 304 Hamilton Hall, 1645 Neil Ave, The Ohio State University College of Medicine, Columbus, OH 43210, USA
    Cardiovasc Res 75:69-78. 2007
    ..The goal of this study was to establish a causal link between CASQ2(D307H) and the CPVT phenotype using an in vivo model...
  33. pmc Differential effects of the peroxynitrite donor, SIN-1, on atrial and ventricular myocyte electrophysiology
    Ingrid M Bonilla
    College of Pharmacy, Division of Pharmacology, The Ohio State University, Columbus, OH 43210, USA
    J Cardiovasc Pharmacol 61:401-7. 2013
    ..A detailed understanding of oxidative modulation of electrophysiology in specific chambers is critical to optimize therapeutic approaches for cardiac diseases...
  34. pmc Synergistic interactions between Ca2+ entries through L-type Ca2+ channels and Na+-Ca2+ exchanger in normal and failing rat heart
    Serge Viatchenko-Karpinski
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, Ohio State University Medical Center, 473 West 12th Avenue, Columbus, OH 43210 1252, USA
    J Physiol 567:493-504. 2005
    ..In heart failure, this new form of Ca2+ release is diminished and may potentially account for the compromised contractile performance and reduced functional reserve in failing hearts...
  35. pmc 'Ryanopathy': causes and manifestations of RyR2 dysfunction in heart failure
    Andriy E Belevych
    Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
    Cardiovasc Res 98:240-7. 2013
    ..We also discuss the implications of these findings for HF therapy...
  36. pmc Dietary omega-3 fatty acids promote arrhythmogenic remodeling of cellular Ca2+ handling in a postinfarction model of sudden cardiac death
    Andriy E Belevych
    Dorothy M Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States of America Department of Physiology and Cell Biology, College of Medicine, The Ohio State University, Columbus, Ohio, United States of America
    PLoS ONE 8:e78414. 2013
    ..Furthermore, dietary n-3 PUFAs increase vulnerability of ventricular myocytes to cellular arrhythmia in post-MI VF- hearts by destabilizing intracellular Ca(2+) handling. ..
  37. pmc Ryanodine receptor phosphorylation by oxidized CaMKII contributes to the cardiotoxic effects of cardiac glycosides
    Hsiang Ting Ho
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA
    Cardiovasc Res 101:165-74. 2014
    ..However, the specific pathway(s) of ROS production and the subsequent downstream molecular events that mediate CG-dependent arrhythmogenesis remain to be defined...
  38. ncbi request reprint Contractile parameters and occurrence of alternans in isolated rat myocardium at supra-physiological stimulation frequency
    Jessica L Slabaugh
    Department of Physiology and Cell Biology, The Ohio State University, Columbus, 43210 1218, USA
    Am J Physiol Heart Circ Physiol 302:H2267-75. 2012
    ....
  39. pmc Chain-reaction Ca(2+) signaling in the heart
    Sandor Gyorke
    Department of Physiology and Cell Biology and OSU Dorothy M Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH, USA
    J Clin Invest 117:1758-62. 2007
    ..In the context of these findings and other recent reports studying CASQ2 mutations, we discuss how CASQ2 influences the properties of Ca(2+)-dependent regulation of RyR2 and how this contributes to cardiac arrhythmogenesis...
  40. doi request reprint miRNAs got rhythm
    Terry S Elton
    Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA
    Life Sci 88:373-83. 2011
    ..In this review we summarize the basic mechanisms of action of miRNAs as they are related to cardiac arrhythmia and address the potential for miRNAs to be therapeutically manipulated in the treatment of arrhythmias...
  41. pmc The calcium-sensing receptor is necessary for the rapid development of hypercalcemia in human lung squamous cell carcinoma
    GWENDOLEN LORCH
    Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210, USA
    Neoplasia 13:428-38. 2011
    ....
  42. pmc The catecholaminergic polymorphic ventricular tachycardia mutation R33Q disrupts the N-terminal structural motif that regulates reversible calsequestrin polymerization
    Naresh C Bal
    Department of Physiology and Cell Biology, The Ohio State University College of Medicine, and The Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA
    J Biol Chem 285:17188-96. 2010
    ..This study provides new mechanistic insight into the functional effects of the R33Q mutation and its potential role in CPVT...
  43. pmc Regulation of myocyte contraction via neuronal nitric oxide synthase: role of ryanodine receptor S-nitrosylation
    Honglan Wang
    Department of Physiology and Cell Biology, Ohio State University, 1645 Neil Avenue, Columbus, OH 43210, USA
    J Physiol 588:2905-17. 2010
    ..These data suggest that NOS1 signalling increases RyR2 activity via S-nitrosylation, which contributes to the NOS1-induced positive inotropic effect. Thus, RyR2 is an important end target of NOS1...
  44. pmc Nitric oxide synthases and atrial fibrillation
    Ingrid M Bonilla
    College of Pharmacy, The Ohio State University Columbus, OH, USA
    Front Physiol 3:105. 2012
    ..Therapeutic approaches to reduce atrial fibrillation by modulation of NOS activity may be beneficial, although further investigation of this strategy is needed...
  45. ncbi request reprint Upregulation of adenosine A1 receptors facilitates sinoatrial node dysfunction in chronic canine heart failure by exacerbating nodal conduction abnormalities revealed by novel dual-sided intramural optical mapping
    Qing Lou
    From the Department of Physiology and Cell Biology Q L, B J H, O F, T A C, A K, N L, L T H, A v G, G E B, P J M, S G, B J B, V V F, Davis Heart and Lung Research Institute Q L, A K, G E B, R W, P J M, S G, B J B, C A C, V V F, and Department of Internal Medicine R W, P J M, The Ohio State University Wexner Medical Center, Columbus, OH Mental Health Research Institute and National Research Tomsk Polytechnic University, Tomsk, Russia O F and College of Pharmacy, The Ohio State University, Columbus C A C
    Circulation 130:315-24. 2014
    ..We aimed to examine the role of adenosine in SAN dysfunction and tachy-brady arrhythmias in chronic HF...
  46. pmc Advanced glycation end product cross-link breaker attenuates diabetes-induced cardiac dysfunction by improving sarcoplasmic reticulum calcium handling
    Allyson L Kranstuber
    College of Pharmacy, The Ohio State University Columbus, OH, USA
    Front Physiol 3:292. 2012
    ....
  47. pmc Protein phosphatases decrease sarcoplasmic reticulum calcium content by stimulating calcium release in cardiac myocytes
    Dmitry Terentyev
    Texas Tech University Health Sciences Center, 3601 4th Street, Lubbock, TX 79430 6551, USA
    J Physiol 552:109-18. 2003
    ..Our results suggest that increased intracellular phosphatase activity stimulates RyR-mediated SR Ca2+ release leading to depleted SR Ca2+ stores in cardiac myocytes...
  48. ncbi request reprint Catecholaminergic polymorphic ventricular tachycardia-related mutations R33Q and L167H alter calcium sensitivity of human cardiac calsequestrin
    Giorgia Valle
    Department of Experimental Biomedical Sciences, University of Padova, IIM Interuniversity Institute of Myology, CNR Institute of Neurosciences, Viale G Colombo 3, 35121, Padova, Italy
    Biochem J 413:291-303. 2008
    ..Initial molecular events of CPVT pathogenesis begin to unveil and appear to be different depending upon the specific CASQ2 mutation...
  49. ncbi request reprint Clinical phenotype and functional characterization of CASQ2 mutations associated with catecholaminergic polymorphic ventricular tachycardia
    Marina Raffaele di Barletta
    Molecular Cardiology, IRCCS Fondazione Maugeri, University of Pavia, Via Ferrata 8 27100, Pavia, Italy
    Circulation 114:1012-9. 2006
    ..The mechanisms leading to the clinical phenotype are still poorly understood because only 1 CASQ2 mutation has been characterized in vitro...

Research Grants20

  1. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2003
    ....
  2. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 1999
    ....
  3. Ryanodine Receptor Channels in Heart Failure
    Sandor Gyorke; Fiscal Year: 2006
    ..The results of this study will improve our understanding of the mechanisms and role of altered Ca handling in HF. ..
  4. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2007
    ....
  5. Abnormal Intracellular Calcium Release in Heart Failure
    Sandor Gyorke; Fiscal Year: 2007
    ..S. population and is the most common diagnosis in hospitalized patients over the age of 65. We propose to study how abnormalities in the regulation of calcium in the heart muscle contribute to heart failure. ..
  6. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2008
    ....
  7. Abnormal Intracellular Calcium Release in Heart Failure
    Sandor Gyorke; Fiscal Year: 2008
    ..S. population and is the most common diagnosis in hospitalized patients over the age of 65. We propose to study how abnormalities in the regulation of calcium in the heart muscle contribute to heart failure. ..
  8. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2009
    ....
  9. Abnormal Intracellular Calcium Release in Heart Failure
    Sandor Gyorke; Fiscal Year: 2009
    ..S. population and is the most common diagnosis in hospitalized patients over the age of 65. We propose to study how abnormalities in the regulation of calcium in the heart muscle contribute to heart failure. ..
  10. Abnormal Intracellular Calcium Release in Heart Failure
    Sandor Gyorke; Fiscal Year: 2010
    ..S. population and is the most common diagnosis in hospitalized patients over the age of 65. We propose to study how abnormalities in the regulation of calcium in the heart muscle contribute to heart failure. ..
  11. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2006
    ....
  12. Ryanodine Receptor Channels in Heart Failure
    Sandor Gyorke; Fiscal Year: 2005
    ..The results of this study will improve our understanding of the mechanisms and role of altered Ca handling in HF. ..
  13. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2000
    ....
  14. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2001
    ....
  15. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2002
    ....
  16. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2003
    ....
  17. Ryanodine Receptor Channels in Heart Failure
    Sandor Gyorke; Fiscal Year: 2003
    ..The results of this study will improve our understanding of the mechanisms and role of altered Ca handling in HF. ..
  18. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2005
    ....
  19. Ryanodine Receptor Channels in Heart Failure
    Sandor Gyorke; Fiscal Year: 2004
    ..The results of this study will improve our understanding of the mechanisms and role of altered Ca handling in HF. ..
  20. CONTROLLED AND UNCONTROLLABLE CALCIUM RELEASE IN HEART
    Sandor Gyorke; Fiscal Year: 2010
    ..S. This proposal will study how improper regulation of calcium by the muscle cells of the heart contributes to arrhythmias. Information gained from this study may help design better therapies for arrhythmias. ..