Ca2+ currents in compensated hypertrophy and heart failure.
about
Characterization of voltage-dependent sodium and calcium channels in mouse pancreatic A- and B-cells.Cardiomyocyte apoptosis triggered by RAFTK/pyk2 via Src kinase is antagonized by paxillinLeft ventricular hypertrophy: The relationship between the electrocardiogram and cardiovascular magnetic resonance imaging.Increased expression of the auxiliary beta(2)-subunit of ventricular L-type Ca(2)+ channels leads to single-channel activity characteristic of heart failureElectrical and structural remodeling in left ventricular hypertrophy-a substrate for a decrease in QRS voltage?Gene therapies for arrhythmias in heart failure.Growth hormone: a promising treatment for the failing heart?Regulation of cardiac excitation-contraction coupling by action potential repolarization: role of the transient outward potassium current (I(to)).Effects of volatile anesthetics on cardiac ion channels.Pathogenesis of dilated cardiomyopathy: molecular, structural, and population analyses in tropomodulin-overexpressing transgenic mice.Mechanisms of ventricular arrhythmias: a dynamical systems-based perspective.Identification of Glycosylation Sites Essential for Surface Expression of the CaVα2δ1 Subunit and Modulation of the Cardiac CaV1.2 Channel Activity.Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes.Inactivation of Myosin binding protein C homolog in zebrafish as a model for human cardiac hypertrophy and diastolic dysfunction.Transgenic simulation of human heart failure-like L-type Ca2+-channels: implications for fibrosis and heart rate in mice.Loss of β-adrenergic-stimulated phosphorylation of CaV1.2 channels on Ser1700 leads to heart failureCalcium pumps in health and disease.Probucol prevents atrial ion channel remodeling in an alloxan-induced diabetes rabbit modelProteolytic cleavage of the hydrophobic domain in the CaVα2δ1 subunit improves assembly and activity of cardiac CaV1.2 channels.Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.Voltage-dependent and frequency-independent inhibition of recombinant Cav3.2 T-type Ca2+ channel by bepridil.Cardiac L-type calcium channel beta-subunits expressed in human heart have differential effects on single channel characteristics.Chronic verapamil treatment remodels ICa,L in mouse ventricle.Negatively charged residues in the first extracellular loop of the L-type CaV1.2 channel anchor the interaction with the CaVα2δ1 auxiliary subunit.Mechanical alternans and restitution in failing SHHF rat left ventricles.Temporal alterations and cellular mechanisms of transmural repolarization during progression of mouse cardiac hypertrophy and failure.Cav3.2 subunit underlies the functional T-type Ca2+ channel in murine hearts during the embryonic period.Physiology and analysis of the electrocardiographic T wave in mice.Pediatric Dilated Cardiomyopathy-Associated LRRC10 (Leucine-Rich Repeat-Containing 10) Variant Reveals LRRC10 as an Auxiliary Subunit of Cardiac L-Type Ca2+ Channels.Conservation of cardiac L-type Ca2+ channels and their regulation in Drosophila: A novel genetically-pliable channelopathic model.Caveolin 3-dependent loss of t-tubular ICa during hypertrophy and heart failure in mice.
P2860
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P2860
Ca2+ currents in compensated hypertrophy and heart failure.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Ca2+ currents in compensated hypertrophy and heart failure.
@en
type
label
Ca2+ currents in compensated hypertrophy and heart failure.
@en
prefLabel
Ca2+ currents in compensated hypertrophy and heart failure.
@en
P2093
P1476
Ca2+ currents in compensated hypertrophy and heart failure
@en
P2093
P304
P356
10.1016/S0008-6363(97)00273-3
P577
1998-02-01T00:00:00Z