A caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility. - Wikidata - awgldk - TriplyDB

A caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility.

A caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility.

http://www.wikidata.org/entity/Q42550135

about

Targeting protein-protein interactions in complexes organized by A kinase anchoring proteins L-type calcium channel targeting and local signalling in cardiac myocytes Popeye domain containing 1 (Popdc1/Bves) is a caveolae-associated protein involved in ischemia tolerance A compartmentalized mathematical model of the β1-adrenergic signaling system in mouse ventricular myocytes Microdomain-Specific Modulation of L-Type Calcium Channels Leads to Triggered Ventricular Arrhythmia in Heart Failure.Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression.Microdomain-specific localization of functional ion channels in cardiomyocytes: an emerging concept of local regulation and remodelling.Modulation of caveolins, integrins and plasma membrane repair proteins in anthracycline-induced heart failure in rabbits.β-Adrenergic receptor-mediated transactivation of epidermal growth factor receptor decreases cardiomyocyte apoptosis through differential subcellular activation of ERK1/2 and Akt.Volume overload induces differential spatiotemporal regulation of myocardial soluble guanylyl cyclase in eccentric hypertrophy and heart failure The gut hormone ghrelin partially reverses energy substrate metabolic alterations in the failing heart.Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction Bio-inspired voltage-dependent calcium channel blockers TRPC3 contributes to regulation of cardiac contractility and arrhythmogenesis by dynamic interaction with NCX1.Cardiac T-Tubule Microanatomy and Function.Identification of caveolar resident proteins in ventricular myocytes using a quantitative proteomic approach: dynamic changes in caveolar composition following adrenoceptor activation.The Ca(2+)-activated cation channel TRPM4 is a negative regulator of angiotensin II-induced cardiac hypertrophy.Caveolin-3 Overexpression Attenuates Cardiac Hypertrophy via Inhibition of T-type Ca2+ Current Modulated by Protein Kinase Cα in Cardiomyocytes Caveolin as a potential drug target for cardiovascular protection.STIM1 elevation in the heart results in aberrant Ca²⁺ handling and cardiomyopathy Caveolins: targeting pro-survival signaling in the heart and brain.Direct Evidence for Microdomain-Specific Localization and Remodeling of Functional L-Type Calcium Channels in Rat and Human Atrial Myocytes.Capturing single L-type Ca(2+) channel function with optics Chronic β1-adrenergic blockade enhances myocardial β3-adrenergic coupling with nitric oxide-cGMP signaling in a canine model of chronic volume overload: new insight into mechanisms of cardiac benefit with selective β1-blocker therapy.A Tension-Based Model Distinguishes Hypertrophic versus Dilated Cardiomyopathy.AKAP150 participates in calcineurin/NFAT activation during the down-regulation of voltage-gated K(+) currents in ventricular myocytes following myocardial infarction.Caveolin-3 suppresses late sodium current by inhibiting nNOS-dependent S-nitrosylation of SCN5A.Similar molecular determinants on Rem mediate two distinct modes of inhibition of CaV1.2 channels.Manipulating L-type calcium channels in cardiomyocytes using split-intein protein transsplicing Aberrant Splicing Promotes Proteasomal Degradation of L-type CaV1.2 Calcium Channels by Competitive Binding for CaVβ Subunits in Cardiac Hypertrophy.Rad GTPase deletion increases L-type calcium channel current leading to increased cardiac contraction.An association of metabolic syndrome constellation with cellular membrane caveolae Phosphorylation of Ser1928 mediates the enhanced activity of the L-type Ca2+ channel Cav1.2 by the β2-adrenergic receptor in neurons.Visualizing CaMKII and CaM activity: a paradigm of compartmentalized signaling Regulation of voltage-dependent calcium channels by RGK proteins.Ion channel engineering: perspectives and strategies.Calcineurin signaling in the heart: The importance of time and place.Superresolution imaging--caveolae, caveolins, mitochondria, and function in heart Imatinib activates pathological hypertrophy by altering myocyte calcium regulation.Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling

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P2860

A caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility.

http://www.wikidata.org/entity/Q42550135

description

2012 nî lūn-bûn

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2012年论文

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2012年论文

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name

A caveolae-targeted L-type Ca² ...... educing cardiac contractility.

@en

A caveolae-targeted L-type Ca² ...... educing cardiac contractility.

@nl

type

label

A caveolae-targeted L-type Ca² ...... educing cardiac contractility.

@en

A caveolae-targeted L-type Ca² ...... educing cardiac contractility.

@nl

prefLabel

A caveolae-targeted L-type Ca² ...... educing cardiac contractility.

@en

A caveolae-targeted L-type Ca² ...... educing cardiac contractility.

@nl

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CIRCRESAHA.111.264028

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Circulation Research

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A caveolae-targeted L-type Ca² ...... educing cardiac contractility.

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Baohua Yang

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Catherine A Makarewich

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Hongyu Zhang

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Hui Gao

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Remus M Berretta

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Robert N Correll

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Steven R Houser

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Victor Rizzo

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P2860

A calcineurin-dependent transcriptional pathway for cardiac hypertrophy

Identification of peptide and protein ligands for the caveolin-scaffolding domain. Implications for the interaction of caveolin with caveolae-associated proteins

Caveolin-3 is adjacent to a group of extradyadic ryanodine receptors

Localization of cardiac L-type Ca(2+) channels to a caveolar macromolecular signaling complex is required for beta(2)-adrenergic regulation

Molecular mechanisms, and selective pharmacological rescue, of Rem-inhibited CaV1.2 channels in heart.

Plasma membrane targeting is essential for Rem-mediated Ca2+ channel inhibition.

CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo.

Calcium-calcineurin signaling in the regulation of cardiac hypertrophy.

Ca2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failure

Calcium cycling and signaling in cardiac myocytes.

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669-674

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10.1161/CIRCRESAHA.111.264028

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5

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110

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Jeffery D. Molkentin

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2012-02-02T00:00:00Z

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221803508

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22302787

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3324037

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