Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction - Wikidata - wikimedia - TriplyDB

Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction

Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction

http://www.wikidata.org/entity/Q28261916

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Gene therapy for cardiovascular disease: advances in vector development, targeting, and delivery for clinical translation Mechanisms of altered Ca²⁺ handling in heart failure Post-translational S-Nitrosylation Is an Endogenous Factor Fine Tuning the Properties of Human S100A1 Protein Adeno-associated virus-mediated gene therapy in cardiovascular disease S100A1 in human heart failure: lack of recovery following left ventricular assist device support Cardiac AAV9-S100A1 gene therapy rescues post-ischemic heart failure in a preclinical large animal model S100A1 and calmodulin regulation of ryanodine receptor in striated muscle S100A1 genetically targeted therapy reverses dysfunction of human failing cardiomyocytes.S100A1 in cardiovascular health and disease: closing the gap between basic science and clinical therapy Targeting S100A1 in heart failure S100A1 binds to the calmodulin-binding site of ryanodine receptor and modulates skeletal muscle excitation-contraction coupling S100A1: Structure, Function, and Therapeutic Potential S100A1: A novel and essential molecular component for postischemic angiogenesis S100A1: a multifaceted therapeutic target in cardiovascular disease Small and large animal models in cardiac contraction research: advantages and disadvantages G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure.Orai1 deficiency leads to heart failure and skeletal myopathy in zebrafish S100A1: a regulator of striated muscle sarcoplasmic reticulum Ca2+ handling, sarcomeric, and mitochondrial function Effects of cardiac-restricted overexpression of the A(2A) adenosine receptor on adriamycin-induced cardiotoxicity Cardioprotection of controlled and cardiac-specific over-expression of A(2A)-adenosine receptor in the pressure overload A novel and efficient model of coronary artery ligation and myocardial infarction in the mouse.Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death.Myocardial injury after ischemia-reperfusion in mice deficient in Akt2 is associated with increased cardiac macrophage density S100A1 as a Potential Diagnostic Biomarker for Assessing Cardiotoxicity and Implications for the Chemotherapy of Certain Cancers.Bioactive nanoparticles improve calcium handling in failing cardiac myocytes.Liquid jet delivery method featuring S100A1 gene therapy in the rodent model following acute myocardial infarction.S100A1 DNA-based Inotropic Therapy Protects Against Proarrhythmogenic Ryanodine Receptor 2 Dysfunction.S100A1: a novel inotropic regulator of cardiac performance. Transition from molecular physiology to pathophysiological relevance.Altered sarcoplasmic reticulum calcium cycling--targets for heart failure therapy.Immunohistochemical detection of S100A1 in the postmortem diagnosis of acute myocardial infarction.Application of mutated miR-206 target sites enables skeletal muscle-specific silencing of transgene expression of cardiotropic AAV9 vectors.Gene therapy in heart failure.Functions of S100 proteins.S100A1 transgenic treatment of acute heart failure causes proteomic changes in rats.S100A1 Protein Does Not Compete with Calmodulin for Ryanodine Receptor Binding but Structurally Alters the Ryanodine Receptor·Calmodulin Complex.Induced overexpression of Na+/Ca2+ exchanger transgene: altered myocyte contractility, [Ca2+]i transients, SR Ca2+ contents, and action potential duration.Designing heart performance by gene transfer.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.Gene and cytokine therapy for heart failure: molecular mechanisms in the improvement of cardiac function.Joining S100 proteins and migration: for better or for worse, in sickness and in health.

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Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction

http://www.wikidata.org/entity/Q28261916

description

2006 nî lūn-bûn

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2006 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2006年の論文

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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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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Cardiac S100A1 protein levels ...... re after myocardial infarction

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Andrew Remppis

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Arthur M Feldman

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