Sodium channel slow inactivation interferes with open channel block.

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Conservation of alternative splicing in sodium channels reveals evolutionary focus on release from inactivation and structural insights into gating.Hysteresis in voltage-gated channels Toxins That Affect Voltage-Gated Sodium Channels.

P2860

Q38722862-27520782-9CC5-4178-9776-C9802CF64123 Q38968792-08FBBB60-0120-4B2D-9186-DC6D02610067 Q50086110-14B6083F-30B1-44E4-96FD-AC4C932A8CDF

P2860

Sodium channel slow inactivation interferes with open channel block.

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http://www.wikidata.org/entity/Q41505443

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2016 nî lūn-bûn

@nan

2016年の論文

@ja

2016年論文

@yue

2016年論文

@zh-hant

2016年論文

@zh-hk

2016年論文

@zh-mo

2016年論文

@zh-tw

2016年论文

@wuu

2016年论文

@zh

2016年论文

@zh-cn

name

Sodium channel slow inactivation interferes with open channel block.

@en

type

Item

label

Sodium channel slow inactivation interferes with open channel block.

@en

prefLabel

Sodium channel slow inactivation interferes with open channel block.

@en

P1476

Sodium channel slow inactivation interferes with open channel block.

@en

P2093

Andrias O O'Reilly

http://www.w3.org/2001/XMLSchema#string

Esther Eberhardt

http://www.w3.org/2001/XMLSchema#string

Martin Hampl

http://www.w3.org/2001/XMLSchema#string

P2860

Residue-specific effects on slow inactivation at V787 in D2-S6 of Na(v)1.4 sodium channels.

Control of transient, resurgent, and persistent current by open-channel block by Na channel beta4 in cultured cerebellar granule neurons

Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disorders

A mutation in segment I-S6 alters slow inactivation of sodium channels.

Tryptophan substitution of a putative D4S6 gating hinge alters slow inactivation in cardiac sodium channels.

Electrophysiological properties of mutant Nav1.7 sodium channels in a painful inherited neuropathy.

Interactions of local anesthetics with voltage-gated Na+ channels.

Sea-anemone toxin ATX-II elicits A-fiber-dependent pain and enhances resurgent and persistent sodium currents in large sensory neurons.

SCN9A mutations define primary erythermalgia as a neuropathic disorder of voltage gated sodium channels.

Gain-of-function mutation in Nav1.7 in familial erythromelalgia induces bursting of sensory neurons.

P2888

srep25974

P304

25974

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P31

scholarly article

P356

10.1038/SREP25974

http://www.w3.org/2001/XMLSchema#string

P407

English

P478

http://www.w3.org/2001/XMLSchema#string

P50

Angelika Lampert

P577

2016-05-13T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P6179

1044912873

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P698

27174182

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P932

4865801

http://www.w3.org/2001/XMLSchema#string

Sodium channel slow inactivation interferes with open channel block.

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P2860

P2860

Sodium channel slow inactivation interferes with open channel block.

description

name

type

label

prefLabel

P1433

P1476

P2093

P2860

P2888

P304

P31

P356

P407

P478

P50

P577

P6179

P698

P932

P356

P1433

P1476

P2093

P2860

P2888

P304

P31

P356

P407

P478

P50

P577

P6179

P698

P932