Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy. - Wikidata - awgldk - TriplyDB

Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.

Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.

http://www.wikidata.org/entity/Q42592376

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The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential L-type calcium channel targeting and local signalling in cardiac myocytes Calmodulin-dependent protein kinase II: linking heart failure and arrhythmias Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences Targets for therapy in sarcomeric cardiomyopathies Calmodulin binding proteins provide domains of local Ca2+ signaling in cardiac myocytes Methods in cardiomyocyte isolation, culture, and gene transfer.Calcium influx through L-type CaV1.2 Ca2+ channels regulates mandibular development Retinoid acid-induced microRNA-31-5p suppresses myogenic proliferation and differentiation by targeting CamkIIδ.Blunted cardiac beta-adrenergic response as an early indication of cardiac dysfunction in Duchenne muscular dystrophy.Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction Gαq protein carboxyl terminus imitation polypeptide GCIP-27 improves cardiac function in chronic heart failure rats.Different subcellular populations of L-type Ca2+ channels exhibit unique regulation and functional roles in cardiomyocytes Dietary nitrate improves cardiac contractility via enhanced cellular Ca²⁺ signaling.Caveolin-3 Overexpression Attenuates Cardiac Hypertrophy via Inhibition of T-type Ca2+ Current Modulated by Protein Kinase Cα in Cardiomyocytes CXCR4 gene transfer prevents pressure overload induced heart failure Loss of Rad-GTPase produces a novel adaptive cardiac phenotype resistant to systolic decline with aging.STIM1 elevation in the heart results in aberrant Ca²⁺ handling and cardiomyopathy Targeted STIM deletion impairs calcium homeostasis, NFAT activation, and growth of smooth muscle.Aberrant Splicing Promotes Proteasomal Degradation of L-type CaV1.2 Calcium Channels by Competitive Binding for CaVβ Subunits in Cardiac Hypertrophy.Triptolide Upregulates Myocardial Forkhead Helix Transcription Factor p3 Expression and Attenuates Cardiac Hypertrophy.Rad GTPase deletion increases L-type calcium channel current leading to increased cardiac contraction.L-type calcium channel auto-regulation of transcription.G protein-dependent and G protein-independent signaling pathways and their impact on cardiac function.Emerging roles for native Orai Ca2+ channels in cardiovascular disease A pathway and network review on beta-adrenoceptor signaling and beta blockers in cardiac remodeling.L-type Ca2+ channels in heart and brain Rad-deletion Phenocopies Tonic Sympathetic Stimulation of the Heart.Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.β-adrenergic regulation of the L-type Ca2+ channel does not require phosphorylation of α1C Ser1700.Cardiac G-protein-coupled receptor kinase 2 ablation induces a novel Ca2+ handling phenotype resistant to adverse alterations and remodeling after myocardial infarction.Adrenergic signaling controls RGK-dependent trafficking of cardiac voltage-gated L-type Ca2+ channels through PKD1.Persistent increases in Ca(2+) influx through Cav1.2 shortens action potential and causes Ca(2+) overload-induced afterdepolarizations and arrhythmias.Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signaling Resistance to pathologic cardiac hypertrophy and reduced expression of CaV1.2 in Trpc3-depleted mice.A caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility.Cardiotoxic and cardioprotective features of chronic β-adrenergic signaling.Alternative Splicing of L-type CaV1.2 Calcium Channels: Implications in Cardiovascular Diseases.Molecular mechanisms and physiological relevance of RGK proteins in the heart.Role of STIM1 (Stromal Interaction Molecule 1) in Hypertrophy-Related Contractile Dysfunction.

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Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.

http://www.wikidata.org/entity/Q42592376

description

2010 nî lūn-bûn

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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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2010年论文

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2010年论文

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name

Calcium influx through Cav1.2 ...... cal cardiomyocyte hypertrophy.

@en

Calcium influx through Cav1.2 ...... cal cardiomyocyte hypertrophy.

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type

label

Calcium influx through Cav1.2 ...... cal cardiomyocyte hypertrophy.

@en

Calcium influx through Cav1.2 ...... cal cardiomyocyte hypertrophy.

@nl

prefLabel

Calcium influx through Cav1.2 ...... cal cardiomyocyte hypertrophy.

@en

Calcium influx through Cav1.2 ...... cal cardiomyocyte hypertrophy.

@nl

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J.YJMCC.2010.11.012

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Journal of Molecular and Cellular Cardiology

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Calcium influx through Cav1.2 ...... cal cardiomyocyte hypertrophy.

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Andrea D Eckhart

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Christopher Szeto

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David M Harris

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Hiroyuki Nakayama

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Hongyu Zhang

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Kathryn Stockbower

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Mingxin Tang

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Remus M Berretta

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Steven R Houser

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Walter J Koch

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P2860

Physical and functional interaction between calcineurin and the cardiac L-type Ca2+ channel

Regulation of cardiac hypertrophy by intracellular signalling pathways

TRPC3 and TRPC6 are essential for angiotensin II-induced cardiac hypertrophy.

Increased expression of the auxiliary beta(2)-subunit of ventricular L-type Ca(2)+ channels leads to single-channel activity characteristic of heart failure

TRPC1 channels are critical for hypertrophic signaling in the heart.

Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.

The L-type calcium channel inhibitor diltiazem prevents cardiomyopathy in a mouse model.

Endothelin-1-stimulated InsP3-induced Ca2+ release is a nexus for hypertrophic signaling in cardiac myocytes.

A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension.

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

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460-470

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10.1016/J.YJMCC.2010.11.012

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3

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Jeffery D. Molkentin

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2010-11-25T00:00:00Z

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49639623

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21111744

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