Triadin deletion induces impaired skeletal muscle function
about
Absence of triadin, a protein of the calcium release complex, is responsible for cardiac arrhythmia with sudden death in humanTriadin regulation of the ryanodine receptor complexReview of RyR1 pathway and associated pathomechanismsCalsequestrin (CASQ1) rescues function and structure of calcium release units in skeletal muscles of CASQ1-null miceCaveolin 3 is associated with the calcium release complex and is modified via in vivo triadin modification.Excitation-contraction coupling and minor triadic proteins in low-frequency fatigueTriadin/Junctin double null mouse reveals a differential role for Triadin and Junctin in anchoring CASQ to the jSR and regulating Ca(2+) homeostasis.Reduced gain of excitation-contraction coupling in triadin-null myotubes is mediated by the disruption of FKBP12/RyR1 interactionCyclization of the intrinsically disordered α1S dihydropyridine receptor II-III loop enhances secondary structure and in vitro function.A new cytoplasmic interaction between junctin and ryanodine receptor Ca2+ release channels.On the footsteps of Triadin and its role in skeletal muscleThe couplonopathies: A comparative approach to a class of diseases of skeletal and cardiac muscle.Dietary selenium augments sarcoplasmic calcium release and mechanical performance in mice.Enhancement of neuromuscular dynamics and strength behavior using extremely low magnitude mechanical signals in mice.Functional Characterization of a Central Core Disease RyR1 Mutation (p.Y4864H) Associated with Quantitative Defect in RyR1 Protein.Ryanodine receptor studies using genetically engineered mice.Reciprocal dihydropyridine and ryanodine receptor interactions in skeletal muscle activation.Core skeletal muscle ryanodine receptor calcium release complex.Excitation-Contraction Coupling Alterations in Myopathies.Distinct regions of triadin are required for targeting and retention at the junctional domain of the sarcoplasmic reticulum.Cannabinoid signalling inhibits sarcoplasmic Ca2+ release and regulates excitation-contraction coupling in mammalian skeletal muscle.Congenital myopathy associated with the triadin knockout syndrome.RyR1 deficiency in congenital myopathies disrupts excitation-contraction coupling.Fluvastatin-induced alterations of skeletal muscle function in hypercholesterolaemic rats.Deletion of the microtubule-associated protein 6 (MAP6) results in skeletal muscle dysfunction
P2860
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P2860
Triadin deletion induces impaired skeletal muscle function
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 19 October 2009
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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
Triadin deletion induces impaired skeletal muscle function
@en
Triadin deletion induces impaired skeletal muscle function.
@nl
type
label
Triadin deletion induces impaired skeletal muscle function
@en
Triadin deletion induces impaired skeletal muscle function.
@nl
prefLabel
Triadin deletion induces impaired skeletal muscle function
@en
Triadin deletion induces impaired skeletal muscle function.
@nl
P2093
P2860
P356
P1476
Triadin deletion induces impaired skeletal muscle function
@en
P2093
Annie Schweitzer
Benoit Giannesini
David Bendahan
Isabelle Marty
Jacques Brocard
Joël Lunardi
Julie Brocard
Julien Fauré
Karine Pernet-Gallay
Laszlo Csernoch
P2860
P304
34918-34929
P356
10.1074/JBC.M109.022442
P407
P577
2009-10-19T00:00:00Z