Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice. - Wikidata - awgldk - TriplyDB

Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.

Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.

http://www.wikidata.org/entity/Q40053441

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The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential Signaling effectors underlying pathologic growth and remodeling of the heart Origin of cardiomyocytes in the adult heart Calcium signaling regulates ventricular hypertrophy during development independent of contraction or blood flow.Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria Loss of MicroRNA-155 protects the heart from pathological cardiac hypertrophy Pathophysiology of Heart Failure.Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy Basal and β-adrenergic regulation of the cardiac calcium channel CaV1.2 requires phosphorylation of serine 1700 Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression.Dynamic alterations in the CaV1.2/CaM/CaMKII signaling pathway in the left ventricular myocardium of ischemic rat hearts Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia.Cardiac ablation of Rheb1 reduces sodium currents in infant mice Interleukin-1β reduces L-type Ca2+ current through protein kinase Cϵ activation in mouse heart.Cardiac T-Tubule Microanatomy and Function.Functional role of Calstabin2 in age-related cardiac alterations.Altered myocardial calcium cycling and energetics in heart failure--a rational approach for disease treatment.Polycystin-1 Is a Cardiomyocyte Mechanosensor That Governs L-Type Ca2+ Channel Protein Stability Prolonged action potential duration in cardiac ablation of PDK1 mice The Mitochondrial Calcium Uniporter Selectively Matches Metabolic Output to Acute Contractile Stress in the Heart Cacna1c (Cav1.2) Modulates Electroencephalographic Rhythm and Rapid Eye Movement Sleep Recovery.Mutation of the calmodulin binding motif IQ of the L-type Ca(v)1.2 Ca2+ channel to EQ induces dilated cardiomyopathy and death.Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia-reperfusion injury.STIM1 elevation in the heart results in aberrant Ca²⁺ handling and cardiomyopathy Anchoring proteins as regulators of signaling pathways.Cardiac remodeling in the mouse model of Marfan syndrome develops into two distinctive phenotypes Altered sarcoplasmic reticulum calcium cycling--targets for heart failure therapy.BIN1 regulates dynamic t-tubule membrane.MicroRNA-22 regulates cardiac hypertrophy and remodeling in response to stress Alterations in ryanodine receptors and related proteins in heart failure Depressed pacemaker activity of sinoatrial node myocytes contributes to the age-dependent decline in maximum heart rate.Aberrant Splicing Promotes Proteasomal Degradation of L-type CaV1.2 Calcium Channels by Competitive Binding for CaVβ Subunits in Cardiac Hypertrophy.Loss of β-adrenergic-stimulated phosphorylation of CaV1.2 channels on Ser1700 leads to heart failure Protein kinetic signatures of the remodeling heart following isoproterenol stimulation.Multilayered regulation of cardiac ion channels.MicroRNA regulation of cardiac conduction and arrhythmias L-type CaV1.2 calcium channels: from in vitro findings to in vivo function.L-type Ca2+ channels in heart and brain PM2.5 exposure in utero contributes to neonatal cardiac dysfunction in mice.Expression of Cav1.3 calcium channel in the human and mouse colon: posttranscriptional inhibition by IFNγ.

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Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.

http://www.wikidata.org/entity/Q40053441

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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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Decreased cardiac L-type Ca²⁺ ...... phy and heart failure in mice.

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Decreased cardiac L-type Ca²⁺ ...... phy and heart failure in mice.

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Decreased cardiac L-type Ca²⁺ ...... phy and heart failure in mice.

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Decreased cardiac L-type Ca²⁺ ...... phy and heart failure in mice.

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Allen J York

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Andrew R Marks

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Franz Hofmann

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Hongyu Zhang

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Ilona Bodi

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Karin Hammer

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Mannix Auger-Messier

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Michelle A Sargent

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Robert N Correll

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Sanjeewa A Goonasekera

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P2860

Calsarcins, a novel family of sarcomeric calcineurin-binding proteins

Cardiac ryanodine receptor phosphorylation by CaM Kinase II: keeping the balance right

Cardiac excitation-contraction coupling

Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum

A calcineurin-dependent transcriptional pathway for cardiac hypertrophy

Calcium oscillations increase the efficiency and specificity of gene expression

Differential activation of transcription factors induced by Ca2+ response amplitude and duration

Calmodulin mediates differential sensitivity of CaMKII and calcineurin to local Ca2+ in cardiac myocytes

Functional embryonic cardiomyocytes after disruption of the L-type alpha1C (Cav1.2) calcium channel gene in the mouse.

Dilated cardiomyopathy with increased SR Ca2+ loading preceded by a hypercontractile state and diastolic failure in the alpha(1C)TG mouse.

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280-290

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10.1172/JCI58227

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1

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122

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Jeffery D. Molkentin

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2011-12-01T00:00:00Z

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22133878

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3248289

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