A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation.
about
Phyla- and Subtype-Selectivity of CgNa, a Na Channel Toxin from the Venom of the Giant Caribbean Sea Anemone Condylactis GiganteaMultiple arrhythmic syndromes in a newborn, owing to a novel mutation in SCN5AHuman sodium channel myotonia: slowed channel inactivation due to substitutions for a glycine within the III-IV linkerMolecular determinants of inactivation within the I-II linker of alpha1E (CaV2.3) calcium channels.Distinctive modulatory effects of five human auxiliary beta2 subunit splice variants on L-type calcium channel gating.A1152D mutation of the Na+ channel causes paramyotonia congenita and emphasizes the role of DIII/S4-S5 linker in fast inactivationSodium channel molecular conformations and antiarrhythmic drug affinityAdaptive evolution of voltage-gated sodium channels: the first 800 million yearsA missense mutation of the Na+ channel alpha II subunit gene Na(v)1.2 in a patient with febrile and afebrile seizures causes channel dysfunctionRole of voltage-gated sodium, potassium and calcium channels in the development of cocaine-associated cardiac arrhythmiasMapping the receptor site for alpha-scorpion toxins on a Na+ channel voltage sensorElimination of rapid potassium channel inactivation by phosphorylation of the inactivation gateRegulation of sodium channel function by bilayer elasticity: the importance of hydrophobic coupling. Effects of Micelle-forming amphiphiles and cholesterolMolecular analysis of the Na+ channel blocking actions of the novel class I anti-arrhythmic agent RSD 921State-dependent trapping of flecainide in the cardiac sodium channelFunctional characterization and cold sensitivity of T1313A, a new mutation of the skeletal muscle sodium channel causing paramyotonia congenita in humansConduction abnormalities and ventricular arrhythmogenesis: The roles of sodium channels and gap junctionsThe hitchhiker's guide to the voltage-gated sodium channel galaxyMolecular pathophysiology and pharmacology of the voltage-sensing module of neuronal ion channelsThe role of late I Na in development of cardiac arrhythmiasCardiac sodium channel Nav1.5 mutations and cardiac arrhythmiaTowards a Unified Theory of Calmodulin Regulation (Calmodulation) of Voltage-Gated Calcium and Sodium ChannelsThree-dimensional solution structure of the sodium channel agonist/antagonist delta-conotoxin TxVIACrystal Structure of a Fibroblast Growth Factor Homologous Factor (FHF) Defines a Conserved Surface on FHFs for Binding and Modulation of Voltage-gated Sodium ChannelsCrystallographic basis for calcium regulation of sodium channelsCrystal structure of a voltage-gated sodium channel in two potentially inactivated statesAtom-by-atom engineering of voltage-gated ion channels: magnified insights into function and pharmacologyStructural Basis for Pharmacology of Voltage-Gated Sodium and Calcium ChannelsTwo tetrodotoxin-resistant sodium channels in human dorsal root ganglion neuronsSodium channel beta1 subunit-mediated modulation of Nav1.2 currents and cell surface density is dependent on interactions with contactin and ankyrinA single residue differentiates between human cardiac and skeletal muscle Na+ channel slow inactivationFunctional expression of Drosophila para sodium channels. Modulation by the membrane protein TipE and toxin pharmacologyCharacterization of the honeybee AmNaV1 channel and tools to assess the toxicity of insecticidesStructure and function of voltage-gated sodium channels at atomic resolution.The VGL-Chanome: A Protein Superfamily Specialized for Electrical Signaling and Ionic HomeostasisModulation of sodium channel inactivation gating by a novel lactam: implications for seizure suppression in chronic limbic epilepsyA pharmacophore derived phenytoin analogue with increased affinity for slow inactivated sodium channels exhibits a desired anticonvulsant profileY3+ block demonstrates an intracellular activation gate for the alpha1G T-type Ca2+ channelVoltage-gated Na+ channels in neuropathic pain.Ultra-slow inactivation in mu1 Na+ channels is produced by a structural rearrangement of the outer vestibule
P2860
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P2860
A cluster of hydrophobic amino acid residues required for fast Na(+)-channel inactivation.
description
1992 nî lūn-bûn
@nan
1992年の論文
@ja
1992年学术文章
@wuu
1992年学术文章
@zh-cn
1992年学术文章
@zh-hans
1992年学术文章
@zh-my
1992年学术文章
@zh-sg
1992年學術文章
@yue
1992年學術文章
@zh
1992年學術文章
@zh-hant
name
A cluster of hydrophobic amino acid residues required for fast Na
@nl
A cluster of hydrophobic amino ...... st Na(+)-channel inactivation.
@en
type
label
A cluster of hydrophobic amino acid residues required for fast Na
@nl
A cluster of hydrophobic amino ...... st Na(+)-channel inactivation.
@en
prefLabel
A cluster of hydrophobic amino acid residues required for fast Na
@nl
A cluster of hydrophobic amino ...... st Na(+)-channel inactivation.
@en
P2093
P2860
P356
P1476
A cluster of hydrophobic amino ...... st Na(+)-channel inactivation.
@en
P2093
P2860
P304
10910-10914
P356
10.1073/PNAS.89.22.10910
P407
P577
1992-11-01T00:00:00Z