Electrophysiological properties of the hypokalaemic periodic paralysis mutation (R528H) of the skeletal muscle alpha 1s subunit as expressed in mouse L cells.
about
Muscle channelopathies and critical points in functional and genetic studies.Omega pore, an alternative ion channel permeation pathway involved in the development of several channelopathiesCa(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channelChannelopathies: ion channel defects linked to heritable clinical disorders.Genetic disorders of neuromuscular ion channels.Recent advances in the pathogenesis and drug action in periodic paralyses and related channelopathies.Voltage-sensor sodium channel mutations cause hypokalemic periodic paralysis type 2 by enhanced inactivation and reduced current.Pathophysiological role of omega pore current in channelopathiesThe primary periodic paralyses: diagnosis, pathogenesis and treatment.A Na+ channel mutation linked to hypokalemic periodic paralysis exposes a proton-selective gating pore.A calcium channel mutant mouse model of hypokalemic periodic paralysisHypokalemic periodic paralysis: a model for a clinical and research approach to a rare disorder.Gating pore currents in DIIS4 mutations of NaV1.4 associated with periodic paralysis: saturation of ion flux and implications for disease pathogenesisMuscle channelopathies: does the predicted channel gating pore offer new treatment insights for hypokalaemic periodic paralysis?Voltage-sensor mutations in channelopathies of skeletal muscle.Neuronal P/Q-type calcium channel dysfunction in inherited disorders of the CNS.Biophysics, pathophysiology, and pharmacology of ion channel gating pores.Elevated resting H(+) current in the R1239H type 1 Hypokalemic Periodic Paralysis mutated Ca(2+) channel.Sodium channel inactivation defects are associated with acetazolamide-exacerbated hypokalemic periodic paralysis.Impairment of skeletal muscle adenosine triphosphate-sensitive K+ channels in patients with hypokalemic periodic paralysisCalcium currents and transients of native and heterologously expressed mutant skeletal muscle DHP receptor alpha1 subunits (R528H)Mechanisms Responsible for ω-Pore Currents in Cav Calcium Channel Voltage-Sensing Domains.Na leak with gating pore properties in hypokalemic periodic paralysis V876E mutant muscle Ca channel.Stac3 enhances expression of human CaV1.1 in Xenopus oocytes and reveals gating pore currents in HypoPP mutant channels.Effects of mutations causing hypokalaemic periodic paralysis on the skeletal muscle L-type Ca2+ channel expressed in Xenopus laevis oocytes.When muscle Ca2+ channels carry monovalent cations through gating pores: insights into the pathophysiology of type 1 hypokalaemic periodic paralysis.
P2860
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P2860
Electrophysiological properties of the hypokalaemic periodic paralysis mutation (R528H) of the skeletal muscle alpha 1s subunit as expressed in mouse L cells.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年学术文章
@wuu
1996年学术文章
@zh-cn
1996年学术文章
@zh-hans
1996年学术文章
@zh-my
1996年学术文章
@zh-sg
1996年學術文章
@yue
1996年學術文章
@zh
1996年學術文章
@zh-hant
name
Electrophysiological propertie ...... as expressed in mouse L cells.
@en
type
label
Electrophysiological propertie ...... as expressed in mouse L cells.
@en
prefLabel
Electrophysiological propertie ...... as expressed in mouse L cells.
@en
P2093
P2860
P1433
P1476
Electrophysiological propertie ...... as expressed in mouse L cells
@en
P2093
P2860
P304
P356
10.1016/0014-5793(96)00173-1
P407
P577
1996-03-01T00:00:00Z