β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes. - Wikidata - thesis-toulmin - TriplyDB

β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.

β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.

http://www.wikidata.org/entity/Q38294845

about

Cyclic stretch of embryonic cardiomyocytes increases proliferation, growth, and expression while repressing Tgf-β signaling Hypothyroidism and its rapid correction alter cardiac remodeling Deletion of low molecular weight protein tyrosine phosphatase (Acp1) protects against stress-induced cardiomyopathy.Increased afterload induces pathological cardiac hypertrophy: a new in vitro model Unique transcriptional profile of sustained ligand-activated preconditioning in pre- and post-ischemic myocardium.Iron overload exacerbates age-associated cardiac hypertrophy in a mouse model of hemochromatosis Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone Alpha-1-adrenergic receptors: targets for agonist drugs to treat heart failure.Metabolic efficiency promotes protection from pressure overload in hearts expressing slow skeletal troponin I.Effect of transverse aortic constriction on cardiac structure, function and gene expression in pregnant rats.Inhibition of hypertrophy is a good therapeutic strategy in ventricular pressure overload.Classic studies of cultured cardiac myocyte hypertrophy: interview with a transformer Transgenic Expression of the Formin Protein Fhod3 Selectively in the Embryonic Heart: Role of Actin-Binding Activity of Fhod3 and Its Sarcomeric Localization during Myofibrillogenesis.Leukemia Inhibitory Factor Enhances Endogenous Cardiomyocyte Regeneration after Myocardial Infarction.Aldosterone and cardiovascular disease: the heart of the matter.Unique mechanistic insights into the beneficial effects of soluble epoxide hydrolase inhibitors in the prevention of cardiac fibrosis.Intraventricular and interventricular cellular heterogeneity of inotropic responses to α(1)-adrenergic stimulation.Antagonism of the thromboxane-prostanoid receptor is cardioprotective against right ventricular pressure overload.Prenatal programming: adverse cardiac programming by gestational testosterone excess.Role of AKAP79/150 protein in β1-adrenergic receptor trafficking and signaling in mammalian cells Cardiac alpha1-adrenergic receptors: novel aspects of expression, signaling mechanisms, physiologic function, and clinical importance American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Discrete effects of A57G-myosin essential light chain mutation associated with familial hypertrophic cardiomyopathy Alpha-1-adrenergic receptors in heart failure: the adaptive arm of the cardiac response to chronic catecholamine stimulation.Myofibroblast-mediated mechanisms of pathological remodelling of the heart.Myofibroblast secretome and its auto-/paracrine signaling.Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting.Atrophied cardiomyocytes and their potential for rescue and recovery of ventricular function.Calcific Aortic Valve Disease: Part 2-Morphomechanical Abnormalities, Gene Reexpression, and Gender Effects on Ventricular Hypertrophy and Its Reversibility.Adrenergic Receptors in Individual Ventricular Myocytes: The Beta-1 and Alpha-1B Are in All Cells, the Alpha-1A Is in a Subpopulation, and the Beta-2 and Beta-3 Are Mostly Absent.Peroxisome proliferator-activated receptor-α expression induces alterations in cardiac myofilaments in a pressure-overload model of hypertrophy.Atrophic cardiomyocyte signaling in hypertensive heart disease Small dedifferentiated cardiomyocytes bordering on microdomains of fibrosis: evidence for reverse remodeling with assisted recovery.MicroRNA profiling predicts a variance in the proliferative potential of cardiac progenitor cells derived from neonatal and adult murine hearts Control of histone H3 phosphorylation by CaMKIIδ in response to haemodynamic cardiac stress.Novel large-particle FACS purification of adult ventricular myocytes reveals accumulation of myosin and actin disproportionate to cell size and proteome in normal post-weaning development.A method to increase reproducibility in adult ventricular myocyte sizing and flow cytometry: Avoiding cell size bias in single cell preparations.Mechanisms of favorable effects of Rho kinase inhibition on myocardial remodeling and systolic function after experimental myocardial infarction in the rat.

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P2860

β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.

http://www.wikidata.org/entity/Q38294845

description

2011 nî lūn-bûn

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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

β-myosin heavy chain is induce ...... maller mouse cardiac myocytes.

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β-myosin heavy chain is induce ...... maller mouse cardiac myocytes.

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β-myosin heavy chain is induce ...... maller mouse cardiac myocytes.

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CIRCRESAHA.111.243410

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Circulation Research

P1476

β-myosin heavy chain is induce ...... maller mouse cardiac myocytes.

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P2093

Bat-Erdene Myagmar

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

Javier E López

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

Manoj C Rodrigo

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

Marty Bigos

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Megan D Montgomery

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Paul C Simpson

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Philip M Swigart

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Stephen Haynam

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P2860

Molecular basis of cardiac performance. Plasticity of the myocardium generated through protein isoform switches

Protooncogene induction and reprogramming of cardiac gene expression produced by pressure overload

Toward transcriptional therapies for the failing heart: chemical screens to modulate genes

Optimizing optical flow cytometry for cell volume-based sorting and analysis.

Skeletal actin mRNA increases in the human heart during ontogenic development and is the major isoform of control and failing adult hearts.

Heterogeneous myocyte enhancer factor-2 (Mef2) activation in myocytes predicts focal scarring in hypertrophic cardiomyopathy.

The cardiac beta-myosin heavy chain isogene is induced selectively in alpha 1-adrenergic receptor-stimulated hypertrophy of cultured rat heart myocytes

Cardiac myosin heavy chain isoform exchange alters the phenotype of cTnT-related cardiomyopathies in mouse hearts.

Alpha1-adrenergic receptors prevent a maladaptive cardiac response to pressure overload.

Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals

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10.1161/CIRCRESAHA.111.243410

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6

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109

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2011-07-21T00:00:00Z

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21778428

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3166391

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