Block of wild-type and inactivation-deficient cardiac sodium channels IFM/QQQ stably expressed in mammalian cells.
about
Role of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmiasDrugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (www.brugadadrugs.org)State-dependent trapping of flecainide in the cardiac sodium channelVoltage-gated sodium channel-associated proteins and alternative mechanisms of inactivation and blockEngineering biosynthetic excitable tissues from unexcitable cells for electrophysiological and cell therapy studies.Inherited and acquired vulnerability to ventricular arrhythmias: cardiac Na+ and K+ channels.Tryptophan scanning of D1S6 and D4S6 C-termini in voltage-gated sodium channelsMultiple modes of ryanodine receptor 2 inhibition by flecainide.Molecular determinants of state-dependent block of voltage-gated sodium channels by pilsicainide.Pharmacogenetics and anti-arrhythmic drug therapy: a theoretical investigation.Sodium channel inactivation: molecular determinants and modulation.Block of inactivation-deficient Na+ channels by local anesthetics in stably transfected mammalian cells: evidence for drug binding along the activation pathway.State-dependent block of wild-type and inactivation-deficient Na+ channels by flecainide.Channel openings are necessary but not sufficient for use-dependent block of cardiac Na(+) channels by flecainide: evidence from the analysis of disease-linked mutations.Multiple pore conformations driven by asynchronous movements of voltage sensors in a eukaryotic sodium channelPersistent human cardiac Na+ currents in stably transfected mammalian cells: Robust expression and distinct open-channel selectivity among Class 1 antiarrhythmics.Multiple targets for flecainide action: implications for cardiac arrhythmogenesis.Local anesthetic inhibition of a bacterial sodium channelDevelopment of recombinant cell line co-expressing mutated Nav1.5, Kir2.1, and hERG for the safety assay of drug candidates.Flecainide sensitivity of a Na channel long QT mutation shows an open-channel blocking mechanism for use-dependent block.Potent block of inactivation-deficient Na+ channels by n-3 polyunsaturated fatty acids.Bupivacaine blocks N-type inactivating Kv channels in the open state: no allosteric effect on inactivation kinetics.Different flecainide sensitivity of hNav1.4 channels and myotonic mutants explained by state-dependent block.The human Nav1.5 F1486 deletion associated with long QT syndrome leads to impaired sodium channel inactivation and reduced lidocaine sensitivity.
P2860
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P2860
Block of wild-type and inactivation-deficient cardiac sodium channels IFM/QQQ stably expressed in mammalian cells.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Block of wild-type and inactiv ...... expressed in mammalian cells.
@en
type
label
Block of wild-type and inactiv ...... expressed in mammalian cells.
@en
prefLabel
Block of wild-type and inactiv ...... expressed in mammalian cells.
@en
P2093
P2860
P1433
P1476
Block of wild-type and inactiv ...... expressed in mammalian cells.
@en
P2093
P2860
P304
P356
10.1016/S0006-3495(00)76538-6
P407
P577
2000-12-01T00:00:00Z