Beta-adrenergic stimulation and myocardial function in the failing heart. - Wikidata - awgldk - TriplyDB

Beta-adrenergic stimulation and myocardial function in the failing heart.

Beta-adrenergic stimulation and myocardial function in the failing heart.

http://www.wikidata.org/entity/Q37358922

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Counteracting Protein Kinase Activity in the Heart: The Multiple Roles of Protein Phosphatases PKA phosphorylation of the small heat-shock protein Hsp20 enhances its cardioprotective effects The relationship between the MMP system, adrenoceptors and phosphoprotein phosphatases Similarly potent inhibition of adenylyl cyclase by P-site inhibitors in hearts from wild type and AC5 knockout mice Small molecule AKAP-protein kinase A (PKA) interaction disruptors that activate PKA interfere with compartmentalized cAMP signaling in cardiac myocytes cGMP Signals Modulate cAMP Levels in a Compartment-Specific Manner to Regulate Catecholamine-Dependent Signaling in Cardiac Myocytes Modeling the effects of β1-adrenergic receptor blockers and polymorphisms on cardiac myocyte Ca2+ handling.Recent advances in the discovery of small molecules targeting exchange proteins directly activated by cAMP (EPAC).Basal and β-adrenergic regulation of the cardiac calcium channel CaV1.2 requires phosphorylation of serine 1700 Protective Role for LPA3 in Cardiac Hypertrophy Induced by Myocardial Infarction but Not by Isoproterenol.Cardiac troponin T, a sarcomeric AKAP, tethers protein kinase A at the myofilaments.Silencing nox4 in the paraventricular nucleus improves myocardial infarction-induced cardiac dysfunction by attenuating sympathoexcitation and periinfarct apoptosis.{beta}1-Adrenergic receptor activation induces mouse cardiac myocyte death through both L-type calcium channel-dependent and -independent pathways.β₂ AR agonists in treatment of chronic heart failure: long path to translation.Integrative modeling of the cardiac ventricular myocyte.Cardiac myocytes and local signaling in nano-domains.Okadaic acid induces matrix metalloproteinase-9 expression in fibroblasts: crosstalk between protein phosphatase inhibition and β-adrenoceptor signalling Cardiac Effects of Attenuating Gsα - Dependent Signaling Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice Pharmacological characterization of 1-nitrosocyclohexyl acetate, a long-acting nitroxyl donor that shows vasorelaxant and antiaggregatory effects.MLP and CARP are linked to chronic PKCα signalling in dilated cardiomyopathy.Divide and conquer: the application of organelle proteomics to heart failure.Targeted gene therapy for the treatment of heart failure.cMyBP-C as a promiscuous substrate: phosphorylation by non-PKA kinases and its potential significance.Gene and cytokine therapy for heart failure: molecular mechanisms in the improvement of cardiac function.A pathway and network review on beta-adrenoceptor signaling and beta blockers in cardiac remodeling.Heart failure-specific changes in protein kinase signalling.Atrial fibrillation and heart failure: cause or effect?I-1-deficiency negatively impacts survival in a cardiomyopathy mouse model.Serine/Threonine Phosphatases in Atrial Fibrillation.Cardiac hyporesponsiveness in severe sepsis is associated with nitric oxide-dependent activation of G protein receptor kinase.Calcium/Calmodulin-Dependent Protein Kinase II Activity Persists During Chronic β-Adrenoceptor Blockade in Experimental and Human Heart Failure.Contractile Defect Caused by Mutation in MYBPC3 Revealed under Conditions Optimized for Human PSC-Cardiomyocyte Function Distinct physiological effects of β1- and β2-adrenoceptors in mouse ventricular myocytes: insights from a compartmentalized mathematical model.Isoproterenol cytotoxicity is dependent on the differentiation state of the cardiomyoblast H9c2 cell line.Mathematical modeling improves EC50 estimations from classical dose-response curves.PPARγ Signaling Mediates the Evolution, Development, Homeostasis, and Repair of the Lung.Constitutively active phosphatase inhibitor-1 improves cardiac contractility in young mice but is deleterious after catecholaminergic stress and with aging.The effect of PKA-mediated phosphorylation of ryanodine receptor on SR Ca2+ leak in ventricular myocytes.Phosphatase-1-inhibitor-1: amplifier or attenuator of catecholaminergic stress?

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P2860

Beta-adrenergic stimulation and myocardial function in the failing heart.

http://www.wikidata.org/entity/Q37358922

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on December 2009

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

Beta-adrenergic stimulation and myocardial function in the failing heart.

@en

Beta-adrenergic stimulation and myocardial function in the failing heart.

@nl

type

label

Beta-adrenergic stimulation and myocardial function in the failing heart.

@en

Beta-adrenergic stimulation and myocardial function in the failing heart.

@nl

prefLabel

Beta-adrenergic stimulation and myocardial function in the failing heart.

@en

Beta-adrenergic stimulation and myocardial function in the failing heart.

@nl

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S10741-008-9132-8

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Heart Failure Reviews

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Beta-adrenergic stimulation and myocardial function in the failing heart.

@en

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Ali El-Armouche

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Thomas Eschenhagen

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P2860

Mutations of the cardiac ryanodine receptor (RyR2) gene in familial polymorphic ventricular tachycardia

Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia

Targeted ablation of the phospholamban gene is associated with markedly enhanced myocardial contractility and loss of beta-agonist stimulation

AKAP-mediated targeting of protein kinase a regulates contractility in cardiac myocytes

Cyclic nucleotide-gated ion channels

beta-adrenergic receptor blockade in chronic heart failure.

beta-adrenergic receptor signaling: an acute compensatory adjustment-inappropriate for the chronic stress of heart failure? Insights from Gsalpha overexpression and other genetically engineered animal models.

In vivo ventricular gene delivery of a beta-adrenergic receptor kinase inhibitor to the failing heart reverses cardiac dysfunction.

Human phospholamban null results in lethal dilated cardiomyopathy revealing a critical difference between mouse and human.

Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats.

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s10741-008-9132-8

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225-241

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scholarly article

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10.1007/S10741-008-9132-8

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4

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14

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2009-12-01T00:00:00Z

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19110970

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