PDE5A suppression of acute beta-adrenergic activation requires modulation of myocyte beta-3 signaling coupled to PKG-mediated troponin I phosphorylation. - Wikidata - wikimedia - TriplyDB

PDE5A suppression of acute beta-adrenergic activation requires modulation of myocyte beta-3 signaling coupled to PKG-mediated troponin I phosphorylation.

PDE5A suppression of acute beta-adrenergic activation requires modulation of myocyte beta-3 signaling coupled to PKG-mediated troponin I phosphorylation.

http://www.wikidata.org/entity/Q30494729

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Heart failure with preserved ejection fraction: emerging drug strategies Nitric oxide synthases in heart failure Compartmentalization of β-adrenergic signals in cardiomyocytes Phosphodiesterases and cardiac cGMP: evolving roles and controversies Inhibition of type 5 phosphodiesterase counteracts β2-adrenergic signalling in beating cardiomyocytes Cyclic nucleotide phosphodiesterase 1A: a key regulator of cardiac fibroblast activation and extracellular matrix remodeling in the heart Stress-dependent dilated cardiomyopathy in mice with cardiomyocyte-restricted inactivation of cyclic GMP-dependent protein kinase I Chronic treatment with long acting phosphodiesterase-5 inhibitor tadalafil alters proteomic changes associated with cytoskeletal rearrangement and redox regulation in Type 2 diabetic hearts.BNP controls early load-dependent regulation of SERCA through calcineurin.Protein kinase G I and heart failure: Shifting focus from vascular unloading to direct myocardial antiremodeling effects.Conserved expression and functions of PDE4 in rodent and human heart.Pressure-overload-induced subcellular relocalization/oxidation of soluble guanylyl cyclase in the heart modulates enzyme stimulation.Redox signaling and cardiac sarcomeres Soluble guanylate cyclase is required for systemic vasodilation but not positive inotropy induced by nitroxyl in the mouse.sGC{alpha}1 mediates the negative inotropic effects of NO in cardiac myocytes independent of changes in calcium handling Cardiac role of cyclic-GMP hydrolyzing phosphodiesterase type 5: from experimental models to clinical trials.Pathological cardiac hypertrophy alters intracellular targeting of phosphodiesterase type 5 from nitric oxide synthase-3 to natriuretic peptide signaling.Identification of murine phosphodiesterase 5A isoforms and their functional characterization in HL-1 cardiac cell line.Molecular Screen Identifies Cardiac Myosin-Binding Protein-C as a Protein Kinase G-Iα Substrate.Old dog, new tricks: novel cardiac targets and stress regulation by protein kinase G.Tadalafil Treatment Delays the Onset of Cardiomyopathy in Dystrophin-Deficient Hearts.Divide and conquer: the application of organelle proteomics to heart failure.Phosphodiesterases and cyclic GMP regulation in heart muscle.Molecular and cellular basis for diastolic dysfunction.Oxidative stress and sarcomeric proteins.Everything you ever wanted to know about phosphodiesterase 5 inhibitors and the heart (but never dared ask): How do they work?Protein kinase G signaling in cardiac pathophysiology: Impact of proteomics on clinical trials.Divergent Effects of miR-181 Family Members on Myocardial Function Through Protective Cytosolic and Detrimental Mitochondrial microRNA Targets.Short-term effects of β2-AR blocker ICI 118,551 on sarcoplasmic reticulum SERCA2a and cardiac function of rats with heart failure.Myocardial remodeling is controlled by myocyte-targeted gene regulation of phosphodiesterase type 5.Protein kinase g iα inhibits pressure overload-induced cardiac remodeling and is required for the cardioprotective effect of sildenafil in vivo.Sildenafil and B-type natriuretic peptide acutely phosphorylate titin and improve diastolic distensibility in vivo.2.1 GHz electromagnetic field does not change contractility and intracellular Ca2+ transients but decreases β-adrenergic responsiveness through nitric oxide signaling in rat ventricular myocytes.The role of cGMP-dependent protein kinase in controlling cardiomyocyte cGMP.Use of a neonatal rat system as a bioincubator to generate adult-like mature cardiomyocytes from human and mouse pluripotent stem cells.Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction.Neonatal Transplantation Confers Maturation of PSC-Derived Cardiomyocytes Conducive to Modeling Cardiomyopathy.Enhanced NO signaling in patients with Takotsubo cardiomyopathy: short-term pain, long-term gain?Selective PDE5A inhibition with sildenafil rescues left ventricular dysfunction, inflammatory immune response and cardiac remodeling in angiotensin II-induced heart failure in vivo.cGMP Signaling in the Cardiovascular System-The Role of Compartmentation and Its Live Cell Imaging.

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P2860

PDE5A suppression of acute beta-adrenergic activation requires modulation of myocyte beta-3 signaling coupled to PKG-mediated troponin I phosphorylation.

http://www.wikidata.org/entity/Q30494729

description

2010 nî lūn-bûn

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2010 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2010 թվականի հունվարին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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PDE5A suppression of acute bet ...... ed troponin I phosphorylation.

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PDE5A suppression of acute bet ...... ed troponin I phosphorylation.

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PDE5A suppression of acute bet ...... ed troponin I phosphorylation.

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PDE5A suppression of acute bet ...... ed troponin I phosphorylation.

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Basic Research in Cardiology

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PDE5A suppression of acute bet ...... ed troponin I phosphorylation.

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David A Kass

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Dong I Lee

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Eiki Takimoto

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Lili A Barouch

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R John Solaro

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Susan Vahebi

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P2860

Differential regulation of endothelial cell permeability by cGMP via phosphodiesterases 2 and 3

The two GAF domains in phosphodiesterase 2A have distinct roles in dimerization and in cGMP binding

Protein kinase C alpha and epsilon phosphorylation of troponin and myosin binding protein C reduce Ca2+ sensitivity in human myocardium

Molecular determinants for cyclic nucleotide binding to the regulatory domains of phosphodiesterase 2A

Cardiac thin filament regulation

A non-equilibrium isoelectric focusing method to determine states of phosphorylation of cardiac troponin I: identification of Ser-23 and Ser-24 as significant sites of phosphorylation by protein kinase C

Expression of slow skeletal troponin I in adult transgenic mouse heart muscle reduces the force decline observed during acidic conditions

Phosphodiesterase type 5 is highly expressed in the hypertrophied human right ventricle, and acute inhibition of phosphodiesterase type 5 improves contractility

Functional role of phosphodiesterase 3 in cardiomyocyte apoptosis: implication in heart failure

Ventricular phosphodiesterase-5 expression is increased in patients with advanced heart failure and contributes to adverse ventricular remodeling after myocardial infarction in mice.

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10.1007/S00395-010-0084-5

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3

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105

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Carlo Gabriele Tocchetti

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2010-01-27T00:00:00Z

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41166995

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1034132302

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20107996

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phosphorylation

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