Voltage sensors in domains III and IV, but not I and II, are immobilized by Na+ channel fast inactivation.
about
Overview of the voltage-gated sodium channel familyNovel functional properties of Ca(2+) channel beta subunits revealed by their expression in adult rat heart cellsFrom foe to friend: using animal toxins to investigate ion channel functionSodium leak channels in neuronal excitability and rhythmic behaviorsResurgent current of voltage-gated Na(+) channelsEnhanced inactivation and acceleration of activation of the sodium channel associated with epilepsy in manA monoclonal antibody that targets a NaV1.7 channel voltage sensor for pain and itch reliefNovel 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 inactivationUnmodified CdSe quantum dots induce elevation of cytoplasmic calcium levels and impairment of functional properties of sodium channels in rat primary cultured hippocampal neuronsSynergetic action of domain II and IV underlies persistent current generation in Nav1.3 as revealed by a tarantula toxin.Use of voltage clamp fluorimetry in understanding potassium channel gating: a review of Shaker fluorescence data.Studies of alpha-helicity and intersegmental interactions in voltage-gated Na+ channels: S2D4.Sodium channel carboxyl-terminal residue regulates fast inactivation.Voltage sensor charge loss accounts for most cases of hypokalemic periodic paralysisAlternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T.The Na channel voltage sensor associated with inactivation is localized to the external charged residues of domain IV, S4.Novel SCN5A mutation in amiodarone-responsive multifocal ventricular ectopy-associated cardiomyopathy.Role of the C-terminal domain in inactivation of brain and cardiac sodium channelsA genetically targetable fluorescent probe of channel gating with rapid kinetics.Kinetic properties and functional dynamics of sodium channels during repetitive spiking in a slow pacemaker neuronEffects of channel cytoplasmic regions on the activation mechanisms of cardiac versus skeletal muscle Na(+) channelsA point mutation in domain 4-segment 6 of the skeletal muscle sodium channel produces an atypical inactivation state.Rapid and slow voltage-dependent conformational changes in segment IVS6 of voltage-gated Na(+) channelsVariable ratio of permeability to gating charge of rBIIA sodium channels and sodium influx in Xenopus oocytes.Mechanism of inactivation gating of human T-type (low-voltage activated) calcium channels.The outermost lysine in the S4 of domain III contributes little to the gating charge in sodium channels.Detecting rearrangements of shaker and NaChBac in real-time with fluorescence spectroscopy in patch-clamped mammalian cells.Ion channel associated diseases: overview of molecular mechanismsThe tarantula toxins ProTx-II and huwentoxin-IV differentially interact with human Nav1.7 voltage sensors to inhibit channel activation and inactivation.Resurgent current and voltage sensor trapping enhanced activation by a beta-scorpion toxin solely in Nav1.6 channel. Significance in mice Purkinje neurons.Functional heterogeneity of the four voltage sensors of a human L-type calcium channelAlpha-scorpion toxin impairs a conformational change that leads to fast inactivation of muscle sodium channels.Structure and function of the voltage sensor of sodium channels probed by a beta-scorpion toxin.Gating pore currents are defects in common with two Nav1.5 mutations in patients with mixed arrhythmias and dilated cardiomyopathy.Voltage-dependent conformational changes in human Ca(2+)- and voltage-activated K(+) channel, revealed by voltage-clamp fluorometry.Voltage-dependent displacement of the scorpion toxin Ts3 from sodium channels and its implication on the control of inactivationDirect evidence that scorpion α-toxins (site-3) modulate sodium channel inactivation by hindrance of voltage-sensor movementsCommon molecular determinants of tarantula huwentoxin-IV inhibition of Na+ channel voltage sensors in domains II and IVMyasthenic syndrome caused by mutation of the SCN4A sodium channel
P2860
Q21999779-40AE3C73-E7B4-4758-A621-E0FC8AEC2EE1Q24642102-A0162816-8D48-437D-9B55-7EED1720ED50Q26864410-7C7E170D-EB27-4154-AF3F-1FF2774AF52DQ26991671-DA0A09A8-2AA3-4225-9B53-5A6D1BB23F20Q27015509-650A3015-D1B5-4654-998A-A57B12D19B1CQ28203362-8C240DBA-F982-4685-9091-32CF19AC93C6Q28240662-EDB7D6B4-6662-4333-B6B3-F04AE9671014Q28345817-2FB1117F-852B-48DD-884D-85709C7F6814Q28363700-6137B56A-6249-480B-A0AE-61E4BA389DF9Q28384797-FC744E47-10F8-4D2B-AD56-81617E2B6D02Q30629019-1E4EF0F3-13D2-462E-BB28-ADDE539FF670Q33467370-6F4E7FF3-B0A5-451F-A8E3-C203CE0FAF69Q33514435-9BFC6E12-0C44-4790-AFD7-20F4D2665259Q33726588-A17EA113-52B5-4BCB-8296-C98E4E06583AQ33763782-50FEBD47-80EE-4444-8B5E-C9DD388F1572Q33796526-8013399B-3552-4BB3-B4B8-07A8C49FBC44Q33869265-634BD8DF-2D32-475F-8BB0-EE23CD7B8E35Q33940611-11F97440-7ECC-4441-9734-E3811BE188E8Q33953193-42D24631-BB1A-469A-88FE-DEA5B8A924BFQ34105807-B687F17D-C061-4A9F-AF93-944EC45A6BB0Q34155647-73BFFB9E-89AC-4585-AB02-462B8FC3DD40Q34171895-8D8714C6-E0CC-4C7C-9FF5-8B204D634460Q34172404-E30A39F0-1ACC-4F45-BAB2-2BB9AA1BA8B2Q34173224-2641F635-99B9-4B02-A0F9-ED06637F731CQ34174237-C9085773-EED6-4B25-B796-72F7EAD65166Q34177582-D8ADF2AF-9FF3-48DD-B8C5-6A5EBFCEBD7DQ34178080-F362298A-2461-40F2-B402-27735ABC07B2Q34186117-FA51DE53-DD7B-4B65-8482-959A86C2CF49Q34311621-5AA3FAA3-2A01-44D0-BA24-09AAE831CFCBQ34359543-50CA6A85-E832-4286-BBDB-2A615F30B49DQ34526433-7A0DCBB1-1AC7-462B-8C2B-0EEBF8BD7786Q34793141-A546070D-1F40-4E3F-94A9-4682E34CE19DQ34802168-3E0EF1AA-DB66-4271-A3B8-E856AD4E0467Q35001630-44D03F4F-A905-4C63-84A8-948630EE28D8Q35014373-6E491490-C915-40A9-AF31-52658F5BA367Q35033825-733D222F-A2E6-4393-A128-36AF37F356A6Q35047477-D7DAF22A-09BB-4638-8C30-E96C828FA107Q35058449-E4478EE2-41FE-49D4-B2FD-15141E3AB5F6Q35144846-61B04189-DF8D-425B-BE4A-68B749E1DCB7Q35163768-EE30EBBD-F736-4207-B68F-B2ABDB26DC5F
P2860
Voltage sensors in domains III and IV, but not I and II, are immobilized by Na+ channel fast inactivation.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
1999年论文
@zh
1999年论文
@zh-cn
name
Voltage sensors in domains III ...... Na+ channel fast inactivation.
@en
type
label
Voltage sensors in domains III ...... Na+ channel fast inactivation.
@en
prefLabel
Voltage sensors in domains III ...... Na+ channel fast inactivation.
@en
P2093
P1433
P1476
Voltage sensors in domains III ...... Na+ channel fast inactivation.
@en
P2093
P356
10.1016/S0896-6273(00)80680-7
P407
P577
1999-01-01T00:00:00Z