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A Coupled SYSTEM of Intracellular Ca2+ Clocks and Surface Membrane Voltage Clocks Controls the Timekeeping Mechanism of the Heartʼs Pacemaker

Circulation research, 2010-03, Vol.106 (4), p.659-673

2010

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Dual Activation of Phosphodiesterase 3 and 4 Regulates Basal Cardiac Pacemaker Function and Beyond

International journal of molecular sciences, 2021-08, Vol.22 (16), p.8414

2021

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Unique Ca2+-Cycling Protein Abundance and Regulation Sustains Local Ca2+ Releases and Spontaneous Firing of Rabbit Sinoatrial Node Cells

International journal of molecular sciences, 2018-07, Vol.19 (8), p.2173

2018

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Dual Activation of Phosphodiesterases 3 and 4 Regulates Basal Spontaneous Beating Rate of Cardiac Pacemaker Cells: Role of Compartmentalization?

Frontiers in physiology, 2018-10, Vol.9, p.1301-1301

2018

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Sarcoplasmic Reticulum Ca2+ Pumping Kinetics Regulates Timing of Local Ca2+ Releases and Spontaneous Beating Rate of Rabbit Sinoatrial Node Pacemaker Cells

Circulation research, 2010-09, Vol.107 (6), p.767-775

2010

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The Emergence of a General Theory of the Initiation and Strength of the Heartbeat

Journal of Pharmacological Sciences, 2006, Vol.100(5), pp.338-369

2006

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Constitutive Phosphodiesterase Activity Restricts Spontaneous Beating Rate of Cardiac Pacemaker Cells by Suppressing Local Ca2+ Releases

Circulation research, 2008-04, Vol.102 (7), p.761-769

2008

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Sarcoplasmic reticulum Ca2+ cycling protein phosphorylation in a physiologic Ca2+ milieu unleashes a high-power, rhythmic Ca2+ clock in ventricular myocytes: Relevance to arrhythmias and bio-pacemaker design

Journal of molecular and cellular cardiology, 2014-01, Vol.66, p.106-115

2014

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Ca²⁺-dependent phosphorylation of Ca²⁺ cycling proteins generates robust rhythmic local Ca²⁺ releases in cardiac pacemaker cells

Science signaling, 2013-01, Vol.6 (260), p.ra6

2013

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The Missing Link in the Mystery of Normal Automaticity of Cardiac Pacemaker Cells

Annals of the New York Academy of Sciences, 2008-03, Vol.1123 (1), p.41-57

2008

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Calcium Cycling Protein Density and Functional Importance to Automaticity of Isolated Sinoatrial Nodal Cells Are Independent of Cell Size

Circulation research, 2007-06, Vol.100 (12), p.1723-1731

2007

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Ca2+-stimulated Basal Adenylyl Cyclase Activity Localization in Membrane Lipid Microdomains of Cardiac Sinoatrial Nodal Pacemaker Cells

The Journal of biological chemistry, 2008-05, Vol.283 (21), p.14461-14468

2008

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Phosphoprotein Phosphatase 1 but Not 2A Activity Modulates Coupled-Clock Mechanisms to Impact on Intrinsic Automaticity of Sinoatrial Nodal Pacemaker Cells

Cells (Basel, Switzerland), 2021-11, Vol.10 (11), p.3106

2021

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Rhythmic Ca2+ Oscillations Drive Sinoatrial Nodal Cell Pacemaker Function to Make the Heart Tick

Annals of the New York Academy of Sciences, 2005-06, Vol.1047 (1), p.138-156

2005

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CaMKII-dependent phosphorylation regulates basal cardiac pacemaker function via modulation of local Ca2+ releases

American journal of physiology. Heart and circulatory physiology, 2016-09, Vol.311 (3), p.H532-H544

2016

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Regulation of basal and reserve cardiac pacemaker function by interactions of cAMP-mediated PKA-dependent Ca2+ cycling with surface membrane channels

Journal of molecular and cellular cardiology, 2009-10, Vol.47 (4), p.456-474

2009

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Diastolic Calcium Release Controls the Beating Rate of Rabbit Sinoatrial Node Cells: Numerical Modeling of the Coupling Process

Biophysical journal, 2004-04, Vol.86 (4), p.2596-2605

2004

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Letter to the editor: "Validating the requirement for beat-to-beat coupling of the Ca2+ clock and M clock in pacemaker cell normal automaticity"

American journal of physiology. Heart and circulatory physiology, 2011-06, Vol.300 (6), p.H2323-4; author reply H2325-6

2011

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Basal Spontaneous Firing of Rabbit Sinoatrial Node Cells Is Regulated by Dual Activation of PDEs (Phosphodiesterases) 3 and 4

Circulation. Arrhythmia and electrophysiology, 2018-06, Vol.11 (6), p.e005896-e005896

2018

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beta-Adrenergic stimulation modulates ryanodine receptor Ca(2+) release during diastolic depolarization to accelerate pacemaker activity in rabbit sinoatrial nodal cells

Circulation research, 2002-01, Vol.90 (1), p.73-79

2002

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Cholinergic receptor signaling modulates spontaneous firing of sinoatrial nodal cells via integrated effects on PKA-dependent Ca2+ cycling and IKACh

American journal of physiology. Heart and circulatory physiology, 2009-09, Vol.297 (3), p.H949-H959

2009

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Ca(2+) -stimulated basal adenylyl cyclase activity localization in membrane lipid microdomains of cardiac sinoatrial nodal pacemaker cells

The Journal of biological chemistry, 2008-05, Vol.283 (21), p.14461-14468

2008

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Membrane Potential Fluctuations Resulting From Submembrane Ca2+ Releases in Rabbit Sinoatrial Nodal Cells Impart an Exponential Phase to the Late Diastolic Depolarization That Controls Their Chronotropic State

Circulation research, 2006-10, Vol.99 (9), p.979-987

2006

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A full range of mouse sinoatrial node AP firing rates requires protein kinase A-dependent calcium signaling

Journal of molecular and cellular cardiology, 2011-11, Vol.51 (5), p.730-739

2011

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Novel Perspectives on the Beating Rate of the Heart

Circulation research, 2002-08, Vol.91 (4), p.e3-e3

2002

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A Coupled SYSTEM of Intracellular Ca2+ Clocks and Surface Membrane Voltage Clocks Controls the Timekeeping Mechanism of the Heartʼs Pacemaker

Dual Activation of Phosphodiesterase 3 and 4 Regulates Basal Cardiac Pacemaker Function and Beyond

Unique Ca2+-Cycling Protein Abundance and Regulation Sustains Local Ca2+ Releases and Spontaneous Firing of Rabbit Sinoatrial Node Cells

Dual Activation of Phosphodiesterases 3 and 4 Regulates Basal Spontaneous Beating Rate of Cardiac Pacemaker Cells: Role of Compartmentalization?

Sarcoplasmic Reticulum Ca2+ Pumping Kinetics Regulates Timing of Local Ca2+ Releases and Spontaneous Beating Rate of Rabbit Sinoatrial Node Pacemaker Cells

The Emergence of a General Theory of the Initiation and Strength of the Heartbeat

Constitutive Phosphodiesterase Activity Restricts Spontaneous Beating Rate of Cardiac Pacemaker Cells by Suppressing Local Ca2+ Releases

Sarcoplasmic reticulum Ca2+ cycling protein phosphorylation in a physiologic Ca2+ milieu unleashes a high-power, rhythmic Ca2+ clock in ventricular myocytes: Relevance to arrhythmias and bio-pacemaker design

Ca²⁺-dependent phosphorylation of Ca²⁺ cycling proteins generates robust rhythmic local Ca²⁺ releases in cardiac pacemaker cells

The Missing Link in the Mystery of Normal Automaticity of Cardiac Pacemaker Cells

Calcium Cycling Protein Density and Functional Importance to Automaticity of Isolated Sinoatrial Nodal Cells Are Independent of Cell Size

Ca2+-stimulated Basal Adenylyl Cyclase Activity Localization in Membrane Lipid Microdomains of Cardiac Sinoatrial Nodal Pacemaker Cells

Phosphoprotein Phosphatase 1 but Not 2A Activity Modulates Coupled-Clock Mechanisms to Impact on Intrinsic Automaticity of Sinoatrial Nodal Pacemaker Cells

Rhythmic Ca2+ Oscillations Drive Sinoatrial Nodal Cell Pacemaker Function to Make the Heart Tick

CaMKII-dependent phosphorylation regulates basal cardiac pacemaker function via modulation of local Ca2+ releases

Regulation of basal and reserve cardiac pacemaker function by interactions of cAMP-mediated PKA-dependent Ca2+ cycling with surface membrane channels

Diastolic Calcium Release Controls the Beating Rate of Rabbit Sinoatrial Node Cells: Numerical Modeling of the Coupling Process

Letter to the editor: "Validating the requirement for beat-to-beat coupling of the Ca2+ clock and M clock in pacemaker cell normal automaticity"

Basal Spontaneous Firing of Rabbit Sinoatrial Node Cells Is Regulated by Dual Activation of PDEs (Phosphodiesterases) 3 and 4

beta-Adrenergic stimulation modulates ryanodine receptor Ca(2+) release during diastolic depolarization to accelerate pacemaker activity in rabbit sinoatrial nodal cells

Cholinergic receptor signaling modulates spontaneous firing of sinoatrial nodal cells via integrated effects on PKA-dependent Ca2+ cycling and IKACh

Ca(2+) -stimulated basal adenylyl cyclase activity localization in membrane lipid microdomains of cardiac sinoatrial nodal pacemaker cells

Membrane Potential Fluctuations Resulting From Submembrane Ca2+ Releases in Rabbit Sinoatrial Nodal Cells Impart an Exponential Phase to the Late Diastolic Depolarization That Controls Their Chronotropic State

A full range of mouse sinoatrial node AP firing rates requires protein kinase A-dependent calcium signaling

Novel Perspectives on the Beating Rate of the Heart

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