Regulation of myocyte contractility by endogenous NO: role of protein phosphatase 2A and protein kinase A-dependent signalling

Regulation of myocyte contractility by endogenous NO: role of protein phosphatase 2A and protein kinase A-dependent signalling

Bibliografiske detaljer
Main Authors:	Zhang, Y, Zhang, M, Sears, C, Redwood, C, El-Armouche, A, Kranias, E, Casadei, B
Format:	Journal article
Udgivet:	2008

Lignende værker

Reduced phospholamban phosphorylation is associated with impaired relaxation in left ventricular myocytes from neuronal NO synthase-deficient mice.
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AMP-Activated protein kinase phosphorylates cardiac troponin i and alters contractility of murine ventricular myocytes
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AMP-activated protein kinase phosphorylates cardiac troponin I and alters contractility of murine ventricular myocytes.
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DISTINCTIVE ROLE FOR PROTEIN PHOSPHATASES AND PROTEIN KINASES IN THE REGULATION OF MYOCARDIAL CONTRACTION BY THE NEURONAL NITRIC OXIDE SYNTHASE
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Cardiac nitric oxide synthase 1 regulates basal and beta-adrenergic contractility in murine ventricular myocytes.
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Is depressed myocyte contractility an early event in the natural history of heart failure?
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Apelin increases cardiac contractility via protein kinase Cε- and extracellular signal-regulated kinase-dependent mechanisms.
af: Ábel Perjés, et al.
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Dilated cardiomyopathy mutations in thin-filament regulatory proteins reduce contractility, suppress systolic Ca²⁺, and activate NFAT and Akt signaling
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Attenuated Subsarcolemmal Protein Phosphatase 2A Activity is Responsible for the Enhanced L-Type Ca Channel Phosphorylation and Contraction in nNOS(-/-) Mice
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Mitochondrial A‐kinase anchoring proteins in cardiac ventricular myocytes
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Mechanical and electrophysiological properties of murine hypertrophied left ventricular myocytes
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Nitric-oxide-mediated regulation of cardiac contractility and stretch responses.
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Caveolae-Independent Activation of Protein Kinase A in Rat Neonatal Myocytes
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Zinc in Regulating Protein Kinases and Phosphatases in Neurodegenerative Diseases
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Is Mitogen‐Activated Protein Kinase Phosphatase 5 a Solution to the Puzzle of the Mitogen‐Activated Protein Kinase Signal in Steatohepatitis?
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Mechanical and electrophysiological properties of left ventricular myocytes in catecholamine-induced hypertrophy in mice
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Superoxide production by left ventricular myocytes in control and hypertrophied hearts
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P387Knock-in mouse model of PRKAG2 cardiomyopathy (R299Q) exhibits altered Ca2+-dependent cardiac contractility and reduced protein kinase A activity.
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Myocardial nNOS-derived NO regulates excitation-contraction coupling via differential and cGMP-independent effects on protein phosphorylation
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nNOS V eNOS mediated regulation of beta adrenergic inotropic and lusitropic responses in left ventricular myocytes
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Frequency-dependent signaling in cardiac myocytes
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A-Kinase Anchoring Proteins in Cardiac Myocytes and Their Roles in Regulating Calcium Cycling
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Age-dependent targeting of protein phosphatase 1 to Ca2+/calmodulin-dependent protein kinase II by spinophilin in mouse striatum.
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Regulated protein kinases and phosphatases in cell cycle decisions
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Regulated protein kinases and phosphatases in cell cycle decisions.
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Multiple functions of protein phosphatases in receptor tyrosine kinase signaling revealed by interactome analysis
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Endogenous nitric oxide formation in cardiac myocytes does not control respiration during β‐adrenergic stimulation
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Image Processing Techniques for Assessing Contractility in Isolated Adult Cardiac Myocytes
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Image Processing Techniques for Assessing Contractility in Isolated Neonatal Cardiac Myocytes
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Protein kinase D participates in cardiomyocyte hypertrophy by regulating extracellular signal-regulated and myocyte enhancer factor 2D
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Effects of DCM mutations in thin filament regulatory proteins on contractile function
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Structural Insights into Protein Regulation by Phosphorylation and Substrate Recognition of Protein Kinases/Phosphatases
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Interaction of kinase-interaction-motif protein tyrosine phosphatases with the mitogen-activated protein kinase ERK2.
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Cardiomyopathy-Causing Mutations in Thin Filament Regulatory Proteins Acutely Affeect Ca2+-Buffering and Ca2+-Dependent Signalling In Situ
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Protein kinase C-dependent dephosphorylation of tyrosine hydroxylase requires the B56δ heterotrimeric form of protein phosphatase 2A.
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