Multiple downstream proarrhythmic targets for calmodulin kinase II: moving beyond an ion channel-centric focus.
about
Atrial fibrillation therapy now and in the future: drugs, biologicals, and ablationCalmodulin kinase II initiates arrhythmogenicity during metabolic acidification in murine heartsOxidized calmodulin kinase II regulates conduction following myocardial infarction: a computational analysis.Na+ channel regulation by Ca2+/calmodulin and Ca2+/calmodulin-dependent protein kinase II in guinea-pig ventricular myocytesTargeting device therapy: genomics of sudden death.Calcium/calmodulin-dependent protein kinase II contributes to cardiac arrhythmogenesis in heart failureOxidized Ca(2+)/calmodulin-dependent protein kinase II triggers atrial fibrillation.Epac activation, altered calcium homeostasis and ventricular arrhythmogenesis in the murine heart.Calcium-calmodulin dependent protein kinase II (CaMKII): a main signal responsible for early reperfusion arrhythmias.Chasing cardiac physiology and pathology down the CaMKII cascadeMechanisms of ventricular arrhythmias: a dynamical systems-based perspective.Ca2+/calmodulin-dependent protein kinase II-dependent remodeling of Ca2+ current in pressure overload heart failure.Calmodulin mutations associated with recurrent cardiac arrest in infants.Cardiac calmodulin kinase: a potential target for drug design.Cardiac ischaemic stress: cardiomyocyte Ca²⁺, sex and sex steroids.Calmodulin in a heartbeat.Ivabradine protects against ventricular arrhythmias in acute myocardial infarction in the rat.The Significance of the Late Na+ Current for Arrhythmia Induction and the Therapeutic Antiarrhythmic Potential of Ranolazine.Pleiotropic mechanisms of action of perhexiline in heart failure.Role of activated CaMKII in abnormal calcium homeostasis and I(Na) remodeling after myocardial infarction: insights from mathematical modeling.Ca(2+) signaling domains responsible for cardiac hypertrophy and arrhythmias.Ca/Calmodulin-dependent Protein Kinase II in Heart Failure.Cardiac overexpression of the human 5-HT4 receptor in mice.Effects of acute and chronic sunitinib treatment on cardiac function and calcium/calmodulin-dependent protein kinase II.Cardiomyocytes with disrupted CFTR function require CaMKII and Ca(2+)-activated Cl(-) channel activity to maintain contraction rate.Preliminary findings of the relationship of lower heart rate variability with military sexual trauma and presumed posttraumatic stress disorder.
P2860
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P2860
Multiple downstream proarrhythmic targets for calmodulin kinase II: moving beyond an ion channel-centric focus.
description
2006 nî lūn-bûn
@nan
2006年の論文
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2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
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2006年论文
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name
Multiple downstream proarrhyth ...... an ion channel-centric focus.
@ast
Multiple downstream proarrhyth ...... an ion channel-centric focus.
@en
type
label
Multiple downstream proarrhyth ...... an ion channel-centric focus.
@ast
Multiple downstream proarrhyth ...... an ion channel-centric focus.
@en
prefLabel
Multiple downstream proarrhyth ...... an ion channel-centric focus.
@ast
Multiple downstream proarrhyth ...... an ion channel-centric focus.
@en
P2860
P1476
Multiple downstream proarrhyth ...... an ion channel-centric focus.
@en
P2093
Mark E Anderson
P2860
P304
P356
10.1016/J.CARDIORES.2006.12.009
P577
2006-12-12T00:00:00Z