The role of the putative inactivation lid in sodium channel gating current immobilization
about
From foe to friend: using animal toxins to investigate ion channel functionNovel mechanism of blocking axonal Na(+) channels by three macrocyclic polyamine analogues and two spider toxinsA single residue differentiates between human cardiac and skeletal muscle Na+ channel slow inactivationThe outermost lysine in the S4 of domain III contributes little to the gating charge in sodium channels.The Scorpion Toxin Tf2 from Tityus fasciolatus Promotes Nav1.3 Opening.Sodium channel inactivation goes with the flowCharge immobilization of skeletal muscle Na+ channels: role of residues in the inactivation linkerSodium channel inactivation: molecular determinants and modulation.Molecular action of lidocaine on the voltage sensors of sodium channelsNeutralization of gating charges in domain II of the sodium channel alpha subunit enhances voltage-sensor trapping by a beta-scorpion toxinTracking voltage-dependent conformational changes in skeletal muscle sodium channel during activation.Immobilizing the moving parts of voltage-gated ion channelsGating charge immobilization in Kv4.2 channels: the basis of closed-state inactivation.Sodium channel inactivation in heart: a novel role of the carboxy-terminal domain.Opening the shaker K+ channel with hanatoxin.Voltage-sensor movements describe slow inactivation of voltage-gated sodium channels I: wild-type skeletal muscle Na(V)1.4.Site-3 toxins and cardiac sodium channels.Extracellular protons inhibit charge immobilization in the cardiac voltage-gated sodium channel.Deconstructing voltage sensor function and pharmacology in sodium channels.Domain IV voltage-sensor movement is both sufficient and rate limiting for fast inactivation in sodium channels.NaV1.4 mutations cause hypokalaemic periodic paralysis by disrupting IIIS4 movement during recovery.Animal toxins influence voltage-gated sodium channel function.Differential modulation of late sodium current by protein kinase A in R1623Q mutant of LQT3.Outward stabilization of the S4 segments in domains III and IV enhances lidocaine block of sodium channels.Outer and central charged residues in DIVS4 of skeletal muscle sodium channels have differing roles in deactivation.Charge immobilization of the voltage sensor in domain IV is independent of sodium current inactivation.Open- and closed-state fast inactivation in sodium channels: differential effects of a site-3 anemone toxin.Outward stabilization of the voltage sensor in domain II but not domain I speeds inactivation of voltage-gated sodium channels.Interaction between fast and ultra-slow inactivation in the voltage-gated sodium channel. Does the inactivation gate stabilize the channel structure?Derivation of Hodgkin-Huxley equations for a Na^{+} channel from a master equation for coupled activation and inactivation.
P2860
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P2860
The role of the putative inactivation lid in sodium channel gating current immobilization
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2000 nî lūn-bûn
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2000年の論文
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2000年学术文章
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2000年学术文章
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2000年学术文章
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2000年学术文章
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2000年学术文章
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2000年學術文章
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2000年學術文章
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2000年學術文章
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name
The role of the putative inactivation lid in sodium channel gating current immobilization
@ast
The role of the putative inactivation lid in sodium channel gating current immobilization
@en
type
label
The role of the putative inactivation lid in sodium channel gating current immobilization
@ast
The role of the putative inactivation lid in sodium channel gating current immobilization
@en
prefLabel
The role of the putative inactivation lid in sodium channel gating current immobilization
@ast
The role of the putative inactivation lid in sodium channel gating current immobilization
@en
P2093
P2860
P356
P1476
The role of the putative inactivation lid in sodium channel gating current immobilization
@en
P2093
P2860
P304
P356
10.1085/JGP.115.5.609
P577
2000-05-01T00:00:00Z