Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger. - Wikidata - awgldk - TriplyDB

Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger.

Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger.

http://www.wikidata.org/entity/Q35964980

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The Na+/Ca²+ exchanger in cardiac ischemia/reperfusion injury A compartmentalized mathematical model of the β1-adrenergic signaling system in mouse ventricular myocytes Regulation of L-type calcium channel by phospholemman in cardiac myocytes.Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity Ca²⁺ entry via Trpm2 is essential for cardiac myocyte bioenergetics maintenance.Targeting cardiomyocyte Ca2+ homeostasis in heart failure.Intracellular trafficking of FXYD1 (phospholemman) and FXYD7 proteins in Xenopus oocytes and mammalian cells.Induced overexpression of Na(+)/Ca(2+) exchanger does not aggravate myocardial dysfunction induced by transverse aortic constriction.BAG3 regulates contractility and Ca(2+) homeostasis in adult mouse ventricular myocytes The second member of transient receptor potential-melastatin channel family protects hearts from ischemia-reperfusion injury.Cardiac Dysfunction in HIV-1 Transgenic Mouse: Role of Stress and BAG3 Development of a high-affinity peptide that prevents phospholemman (PLM) inhibition of the sodium/calcium exchanger 1 (NCX1).Adeno-associated Virus Serotype 9 - Driven Expression of BAG3 Improves Left Ventricular Function in Murine Hearts with Left Ventricular Dysfunction Secondary to a Myocardial Infarction.TRPM2 channels protect against cardiac ischemia-reperfusion injury: role of mitochondria.Induced overexpression of phospholemman S68E mutant improves cardiac contractility and mortality after ischemia-reperfusion.Overexpression of the Na+/K+ ATPase α2 but not α1 isoform attenuates pathological cardiac hypertrophy and remodeling.A new cell-penetrating peptide that blocks the autoinhibitory XIP domain of NCX1 and enhances antiporter activity.Haplo-insufficiency of Bcl2-associated Athanogene 3 in Mice Results in Progressive Left Ventricular Dysfunction, β-Adrenergic Insensitivity and Increased Apoptosis.Methylene blue counteracts cyanide cardiotoxicity: cellular mechanisms.Methylene Blue Counteracts H2S-Induced Cardiac Ion Channel Dysfunction and ATP Reduction.

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Constitutive overexpression of phosphomimetic phospholemman S68E mutant results in arrhythmias, early mortality, and heart failure: potential involvement of Na+/Ca2+ exchanger.

http://www.wikidata.org/entity/Q35964980

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American Journal of Physiology - Heart and Circulatory Physiology

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Arthur M Feldman

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Blaise Z Peterson

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Jeffrey I Joseph

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Jianliang Song

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Joseph Y Cheung

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Jufang Wang

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Tung O Chan

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Walter J Koch

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Xiying Shang

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Xue-Qian Zhang

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P2860

Cytoplasmic tail of phospholemman interacts with the intracellular loop of the cardiac Na+/Ca2+ exchanger

The FXYD gene family of small ion transport regulators or channels: cDNA sequence, protein signature sequence, and expression

Sodium/calcium exchanger: influence of metabolic regulation on ion carrier interactions

Functional adult myocardium in the absence of Na+-Ca2+ exchange: cardiac-specific knockout of NCX1

Effects of Na(+)/Ca(2+) exchanger downregulation on contractility and [Ca(2+)](i) transients in adult rat myocytes

Identification of an endogenous inhibitor of the cardiac Na+/Ca2+ exchanger, phospholemman

Regulation of in vivo cardiac contractility by phospholemman: role of Na+/Ca2+ exchange.

Phospholemman and beta-adrenergic stimulation in the heart.

Serine 68 phospholemman phosphorylation during forskolin-induced swine carotid artery relaxation.

Regulation of cardiac myocyte contractility by phospholemman: Na+/Ca2+ exchange versus Na+ -K+ -ATPase

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