Up-regulation of the inward rectifier K+ current (I K1) in the mouse heart accelerates and stabilizes rotors. - Wikidata - awgldk - TriplyDB

Up-regulation of the inward rectifier K+ current (I K1) in the mouse heart accelerates and stabilizes rotors.

Up-regulation of the inward rectifier K+ current (I K1) in the mouse heart accelerates and stabilizes rotors.

http://www.wikidata.org/entity/Q50708618

about

Altered cardiac electrophysiology and SUDEP in a model of Dravet syndrome CaMKII regulation of cardiac K channels Ionic mechanisms of arrhythmogenesis Ion channel macromolecular complexes in cardiomyocytes: roles in sudden cardiac death A Mathematical Model of Neonatal Rat Atrial Monolayers with Constitutively Active Acetylcholine-Mediated K+ Current Chloroquine terminates stretch-induced atrial fibrillation more effectively than flecainide in the sheep heart Attraction of rotors to the pulmonary veins in paroxysmal atrial fibrillation: a modeling study.Mechanisms underlying the antifibrillatory action of hyperkalemia in Guinea pig hearts.The inward rectifier current inhibitor PA-6 terminates atrial fibrillation and does not cause ventricular arrhythmias in goat and dog models.Transmural heterogeneity of repolarization and Ca2+ handling in a model of mouse ventricular tissue.Regulation of cardiac inward rectifier potassium current (I(K1)) by synapse-associated protein-97.Specific residues of the cytoplasmic domains of cardiac inward rectifier potassium channels are effective antifibrillatory targets.Structural bases for the different anti-fibrillatory effects of chloroquine and quinidine.Genetically engineered excitable cardiac myofibroblasts coupled to cardiomyocytes rescue normal propagation and reduce arrhythmia complexity in heterocellular monolayers Reduced Ventricular Arrhythmogeneity and Increased Electrical Complexity in Normal Exercised Rats.Arrhythmogenic substrate in hearts of rats with monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy.A null mutation of the neuronal sodium channel NaV1.6 disrupts action potential propagation and excitation-contraction coupling in the mouse heart Mathematical modeling mechanisms of arrhythmias in transgenic mouse heart overexpressing TNF-α Dynamic reciprocity of sodium and potassium channel expression in a macromolecular complex controls cardiac excitability and arrhythmia Mechanisms of Atrial Fibrillation - Reentry, Rotors and Reality Universal scaling law of electrical turbulence in the mammalian heart STRUCTURAL AND FUNCTIONAL BASES OF CARDIAC FIBRILLATION. DIFFERENCES AND SIMILARITIES BETWEEN ATRIA AND VENTRICLES.Cardiac fibrillation: from ion channels to rotors in the human heart Nav1.5 N-terminal domain binding to α1-syntrophin increases membrane density of human Kir2.1, Kir2.2 and Nav1.5 channels.Molecular Basis of Functional Myocardial Potassium Channel Diversity.Constitutive Intracellular Na+ Excess in Purkinje Cells Promotes Arrhythmogenesis at Lower Levels of Stress Than Ventricular Myocytes From Mice With Catecholaminergic Polymorphic Ventricular Tachycardia Electrophysiological and structural determinants of electrotonic modulation of repolarization by the activation sequence.A single-cell model of phase-driven control of ventricular fibrillation frequency Electrical remodeling contributes to complex tachyarrhythmias in connexin43-deficient mouse hearts.Information learned from animal models of atrial fibrillation.SAP97 regulates Kir2.3 channels by multiple mechanisms.IK1 heterogeneity affects genesis and stability of spiral waves in cardiac myocyte monolayers.Left versus right atrial difference in dominant frequency, K(+) channel transcripts, and fibrosis in patients developing atrial fibrillation after cardiac surgery.The Major Role of IK1 in Mechanisms of Rotor Drift in the Atria: A Computational Study.Cardiac strong inward rectifier potassium channels.Inward rectifier potassium channels control rotor frequency in ventricular fibrillation Effects of regional mitochondrial depolarization on electrical propagation: implications for arrhythmogenesis.Interpreting genetic effects through models of cardiac electromechanics.Rotors and the dynamics of cardiac fibrillation.miRNA in the regulation of ion channel/transporter expression.

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Up-regulation of the inward rectifier K+ current (I K1) in the mouse heart accelerates and stabilizes rotors.

http://www.wikidata.org/entity/Q50708618

description

2006 nî lūn-bûn

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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2006年學術文章

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name

Up-regulation of the inward re ...... lerates and stabilizes rotors.

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Up-regulation of the inward rectifier K+ current

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type

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Up-regulation of the inward re ...... lerates and stabilizes rotors.

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Up-regulation of the inward rectifier K+ current

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Up-regulation of the inward re ...... lerates and stabilizes rotors.

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Up-regulation of the inward rectifier K+ current

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JPHYSIOL.2006.121475

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The Journal of Physiology

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Up-regulation of the inward re ...... lerates and stabilizes rotors.

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Anatoli N Lopatin

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Karen Vikstrom

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Michelle Zugermayr

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Omer Berenfeld

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Sami F Noujaim

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Sandeep V Pandit

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Sergey Mironov

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P2860

A novel form of short QT syndrome (SQT3) is caused by a mutation in the KCNJ2 gene

Single-Step Method of RNA Isolation by Acid Guanidinium Thiocyanate–Phenol–Chloroform Extraction

Primary structure and functional expression of a mouse inward rectifier potassium channel

Ionic determinants of functional reentry in a 2-D model of human atrial cells during simulated chronic atrial fibrillation.

Altered right atrial excitation and propagation in connexin40 knockout mice.

Spiral waves in two-dimensional models of ventricular muscle: formation of a stationary core.

Inward rectifiers in the heart: an update on I(K1).

The consequences of disrupting cardiac inwardly rectifying K(+) current (I(K1)) as revealed by the targeted deletion of the murine Kir2.1 and Kir2.2 genes.

Functional role of inward rectifier current in heart probed by Kir2.1 overexpression and dominant-negative suppression.

Post-transcriptional regulation of glyceraldehyde-3-phosphate-dehydrogenase gene expression in rat tissues.

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