Oxidized CaMKII causes cardiac sinus node dysfunction in mice. - Wikidata - awgldk - TriplyDB

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

http://www.wikidata.org/entity/Q35572691

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Regulation of CaMKII signaling in cardiovascular disease Atrial Fibrillation and Fibrosis: Beyond the Cardiomyocyte Centric View Fibrosis: a structural modulator of sinoatrial node physiology and dysfunction Ion Channels in the Heart Regulation of thrombosis and vascular function by protein methionine oxidation CaMKII oxidative activation and the pathogenesis of cardiac disease Calmodulin-dependent protein kinase II: linking heart failure and arrhythmias NADPH oxidases in heart failure: poachers or gamekeepers?Mechanisms of altered Ca²⁺ handling in heart failure New therapeutic targets in cardiology: arrhythmias and Ca2+/calmodulin-dependent kinase II (CaMKII)Protein methionine oxidation augments reperfusion injury in acute ischemic stroke Atrial Fibrillation: Epidemiology, Pathophysiology, and Clinical Outcomes.Diabetes increases mortality after myocardial infarction by oxidizing CaMKII Microdomain-Specific Modulation of L-Type Calcium Channels Leads to Triggered Ventricular Arrhythmia in Heart Failure.Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmias Toward a hierarchy of mechanisms in CaMKII-mediated arrhythmia.Three ways to die suddenly: do they all require calcium calmodulin-dependent protein kinase II?Mathematical modeling of physiological systems: an essential tool for discovery.Atrial fibrillation and sinus node dysfunction in human ankyrin-B syndrome: a computational analysis.Oxidized Ca(2+)/calmodulin-dependent protein kinase II triggers atrial fibrillation.Human sinoatrial node structure: 3D microanatomy of sinoatrial conduction pathways.Role of sinoatrial node architecture in maintaining a balanced source-sink relationship and synchronous cardiac pacemaking.Oxidative stress in atrial fibrillation: an emerging role of NADPH oxidase.The multifunctional Ca²⁺/calmodulin-dependent kinase IIδ (CaMKIIδ) regulates arteriogenesis in a mouse model of flow-mediated remodeling.CaMKII is essential for the proasthmatic effects of oxidation.Cycle length restitution in sinoatrial node cells: a theory for understanding spontaneous action potential dynamics.Mitochondrial reprogramming induced by CaMKIIδ mediates hypertrophy decompensation Calsequestrin 2 deletion causes sinoatrial node dysfunction and atrial arrhythmias associated with altered sarcoplasmic reticulum calcium cycling and degenerative fibrosis within the mouse atrial pacemaker complex1.Mitochondrial-targeted antioxidant therapy decreases transforming growth factor-β-mediated collagen production in a murine asthma model The mitochondrial uniporter controls fight or flight heart rate increases.Function and dysfunction of human sinoatrial node Burst pacemaker activity of the sinoatrial node in sodium-calcium exchanger knockout mice.MyD88 mediated inflammatory signaling leads to CaMKII oxidation, cardiac hypertrophy and death after myocardial infarction.Oxidation of CaMKII determines the cardiotoxic effects of aldosterone.Modern perspectives on numerical modeling of cardiac pacemaker cell The multifunctional Ca2+/calmodulin-dependent kinase II regulates vascular smooth muscle migration through matrix metalloproteinase 9.Calmodulin 2 Mutation N98S Is Associated with Unexplained Cardiac Arrest in Infants Due to Low Clinical Penetrance Electrical Disorders Accelerated junctional rhythm and nonalternans repolarization lability precede ventricular tachycardia in Casq2-/- mice.Protective effects of kaempferol against cardiac sinus node dysfunction via CaMKII deoxidization Molecular mechanisms underlying cardiac protein phosphatase 2A regulation in heart.

P2860

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P2860

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

http://www.wikidata.org/entity/Q35572691

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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2011年论文

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2011年论文

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name

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

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Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

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type

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Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

@ast

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

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prefLabel

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

@ast

Oxidized CaMKII causes cardiac sinus node dysfunction in mice.

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P1433

Journal of Clinical Investigation

P1476

Oxidized CaMKII causes cardiac sinus node dysfunction in mice

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P2093

Alexey V Glukhov

http://www.w3.org/2001/XMLSchema#string

Anil Purohit

http://www.w3.org/2001/XMLSchema#string

B Julie He

http://www.w3.org/2001/XMLSchema#string

Dobromir Dobrev

http://www.w3.org/2001/XMLSchema#string

Elizabeth D Luczak

http://www.w3.org/2001/XMLSchema#string

Igor Efimov

http://www.w3.org/2001/XMLSchema#string

J Kevin Donahue

http://www.w3.org/2001/XMLSchema#string

Jinying Yang

http://www.w3.org/2001/XMLSchema#string

Mark E Anderson

http://www.w3.org/2001/XMLSchema#string

Masahiro Ogawa

http://www.w3.org/2001/XMLSchema#string

P2860

The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure

Familial sinus bradycardia associated with a mutation in the cardiac pacemaker channel

Pacemaker channel dysfunction in a patient with sinus node disease

Dysfunction in ankyrin-B-dependent ion channel and transporter targeting causes human sinus node disease

Characterization of a calmodulin kinase II inhibitor protein in brain

A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation

Calmodulin kinase II-mediated sarcoplasmic reticulum Ca2+ leak promotes atrial fibrillation in mice.

Role of CaMKIIdelta phosphorylation of the cardiac ryanodine receptor in the force frequency relationship and heart failure

Sudden death prevention in patients with advanced ventricular dysfunction.

Oxygen, oxidative stress, hypoxia, and heart failure.

P304

3277-3288

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scholarly article

P356

10.1172/JCI57833

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P433

8

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121

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Isabella M Grumbach

Mei-Ling Joiner

P577

2011-07-25T00:00:00Z

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21785215

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3223923

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