Enhanced excitation-coupled calcium entry in myotubes expressing malignant hyperthermia mutation R163C is attenuated by dantrolene.
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Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and DiseaseCa(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channelPharmGKB summary: very important pharmacogene information for RYR1Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicityEccentric muscle contraction and stretching evoke mechanical hyperalgesia and modulate CGRP and P2X(3) expression in a functionally relevant mannerA malignant hyperthermia-inducing mutation in RYR1 (R163C): alterations in Ca2+ entry, release, and retrograde signaling to the DHPR.A malignant hyperthermia-inducing mutation in RYR1 (R163C): consequent alterations in the functional properties of DHPR channelsGreen tea catechins are potent sensitizers of ryanodine receptor type 1 (RyR1).Store-operated Ca2+ entry in malignant hyperthermia-susceptible human skeletal muscle.The cardiac alpha(1C) subunit can support excitation-triggered Ca2+ entry in dysgenic and dyspedic myotubesMalignant hyperthermia susceptibility arising from altered resting coupling between the skeletal muscle L-type Ca2+ channel and the type 1 ryanodine receptorRGK protein-mediated impairment of slow depolarization- dependent Ca2+ entry into developing myotubes.Basal bioenergetic abnormalities in skeletal muscle from ryanodine receptor malignant hyperthermia-susceptible R163C knock-in mice.Functional and biochemical properties of ryanodine receptor type 1 channels from heterozygous R163C malignant hyperthermia-susceptible mice.Localization of the dantrolene-binding sequence near the FK506-binding protein-binding site in the three-dimensional structure of the ryanodine receptor.Malignant hyperthermia and the clinical significance of type-1 ryanodine receptor gene (RYR1) variants: proceedings of the 2013 MHAUS Scientific Conference.Malignant hyperthermia: a pharmacogenetic disorder.Accelerated activation of SOCE current in myotubes from two mouse models of anesthetic- and heat-induced sudden death.Alterations of excitation-contraction coupling and excitation coupled Ca(2+) entry in human myotubes carrying CAV3 mutations linked to rippling muscleCa(2+) permeation and/or binding to CaV1.1 fine-tunes skeletal muscle Ca(2+) signaling to sustain muscle function.Special article: Future directions in malignant hyperthermia research and patient careGene dose influences cellular and calcium channel dysregulation in heterozygous and homozygous T4826I-RYR1 malignant hyperthermia-susceptible muscle.Essential Role of Calmodulin in RyR Inhibition by Dantrolene.Mice expressing T4826I-RYR1 are viable but exhibit sex- and genotype-dependent susceptibility to malignant hyperthermia and muscle damageAntioxidants protect calsequestrin-1 knockout mice from halothane- and heat-induced sudden death.Structural and functional evaluation of branched myofibers lacking intermediate filamentsAlpha2delta1 dihydropyridine receptor subunit is a critical element for excitation-coupled calcium entry but not for formation of tetrads in skeletal myotubesNonspecific sarcolemmal cation channels are critical for the pathogenesis of malignant hyperthermia.Dantrolene-induced inhibition of skeletal L-type Ca2+ current requires RyR1 expression.Halothane modulation of skeletal muscle ryanodine receptors: dependence on Ca2+, Mg2+, and ATP.The skeletal L-type Ca(2+) current is a major contributor to excitation-coupled Ca(2+) entry.Electrically silent divalent cation entries in resting and active voltage-controlled muscle fibersChecking your SOCCs and feet: the molecular mechanisms of Ca2+ entry in skeletal muscle.Malformed mdx myofibers have normal cytoskeletal architecture yet altered EC coupling and stress-induced Ca2+ signaling.Structure-activity relationship of selected meta- and para-hydroxylated non-dioxin like polychlorinated biphenyls: from single RyR1 channels to muscle dysfunction.Baclofen in the Therapeutic of Sequele of Traumatic Brain Injury: Spasticity.Calcium entry in skeletal muscle.The role of store-operated calcium influx in skeletal muscle signaling.The disorders of the calcium release unit of skeletal muscles: what have we learned from mouse models?Muscle weakness in myotonic dystrophy associated with misregulated splicing and altered gating of Ca(V)1.1 calcium channel.
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Enhanced excitation-coupled calcium entry in myotubes expressing malignant hyperthermia mutation R163C is attenuated by dantrolene.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 02 January 2008
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
Enhanced excitation-coupled ca ...... C is attenuated by dantrolene.
@en
Enhanced excitation-coupled ca ...... C is attenuated by dantrolene.
@nl
type
label
Enhanced excitation-coupled ca ...... C is attenuated by dantrolene.
@en
Enhanced excitation-coupled ca ...... C is attenuated by dantrolene.
@nl
prefLabel
Enhanced excitation-coupled ca ...... C is attenuated by dantrolene.
@en
Enhanced excitation-coupled ca ...... C is attenuated by dantrolene.
@nl
P2093
P2860
P356
P1476
Enhanced excitation-coupled ca ...... C is attenuated by dantrolene.
@en
P2093
Chris W Ward
Elaine Cabrales
Gennady Cherednichenko
Isaac N Pessah
José R López
Luke Michaelson
Montserrat Samso
Paul D Allen
P2860
P304
P356
10.1124/MOL.107.043299
P577
2008-01-02T00:00:00Z