Calcium and the damage pathways in muscular dystrophy. - Wikidata - wikimedia - TriplyDB

Calcium and the damage pathways in muscular dystrophy.

Calcium and the damage pathways in muscular dystrophy.

http://www.wikidata.org/entity/Q37710975

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Current and emerging treatment strategies for Duchenne muscular dystrophy Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and Disease Characterization of dystrophin deficient rats: a new model for Duchenne muscular dystrophy Insights into the molecular etiology of exercise-induced inflammation: opportunities for optimizing performance A micropeptide encoded by a putative long noncoding RNA regulates muscle performance Microtubules underlie dysfunction in duchenne muscular dystrophy.New pathobiochemical insights into dystrophinopathy from the proteomics of senescent mdx mouse muscle Enhanced Ca²⁺ influx from STIM1-Orai1 induces muscle pathology in mouse models of muscular dystrophy.Impaired functional communication between the L-type calcium channel and mitochondria contributes to metabolic inhibition in the mdx heart.iNOS ablation does not improve specific force of the extensor digitorum longus muscle in dystrophin-deficient mdx4cv mice.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials Orai1 mediates exacerbated Ca(2+) entry in dystrophic skeletal muscle Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.The role of proteases in excitation-contraction coupling failure in muscular dystrophy.Effects of Dantrolene Therapy on Disease Phenotype in Dystrophin Deficient mdx Mice.Nifedipine treatment reduces resting calcium concentration, oxidative and apoptotic gene expression, and improves muscle function in dystrophic mdx mice.SERCA2a gene transfer improves electrocardiographic performance in aged mdx mice Whole body periodic acceleration is an effective therapy to ameliorate muscular dystrophy in mdx mice.Transgenic overexpression of γ-cytoplasmic actin protects against eccentric contraction-induced force loss in mdx mice SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models.Adaptive strength gains in dystrophic muscle exposed to repeated bouts of eccentric contraction Dystrobrevin controls neurotransmitter release and muscle Ca(2+) transients by localizing BK channels in Caenorhabditis elegans Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage control Low intensity 635 nm diode laser irradiation inhibits fibroblast-myofibroblast transition reducing TRPC1 channel expression/activity: New perspectives for tissue fibrosis treatment.Quantitative evaluation of the beneficial effects in the mdx mouse of epigallocatechin gallate, an antioxidant polyphenol from green tea.Dystrophin and dysferlin double mutant mice: a novel model for rhabdomyosarcoma Increased resting intracellular calcium modulates NF-κB-dependent inducible nitric-oxide synthase gene expression in dystrophic mdx skeletal myotubes Membrane Repair: Mechanisms and Pathophysiology.Focal but reversible diastolic sheet dysfunction reflects regional calcium mishandling in dystrophic mdx mouse hearts.Proteomics reveals drastic increase of extracellular matrix proteins collagen and dermatopontin in the aged mdx diaphragm model of Duchenne muscular dystrophy Muscle RANK is a key regulator of Ca2+ storage, SERCA activity, and function of fast-twitch skeletal muscles.Restricting calcium currents is required for correct fiber type specification in skeletal muscle.Inhibition of iPLA2 β and of stretch-activated channels by doxorubicin alters dystrophic muscle function.Dystrophin restoration therapy improves both the reduced excitability and the force drop induced by lengthening contractions in dystrophic mdx skeletal muscle.Concurrent Label-Free Mass Spectrometric Analysis of Dystrophin Isoform Dp427 and the Myofibrosis Marker Collagen in Crude Extracts from mdx-4cv Skeletal Muscles.X-ROS signaling in the heart and skeletal muscle: stretch-dependent local ROS regulates [Ca²⁺]i.EUK-134 ameliorates nNOSμ translocation and skeletal muscle fiber atrophy during short-term mechanical unloading.Exacerbation of pathology by oxidative stress in respiratory and locomotor muscles with Duchenne muscular dystrophy.The selective BH4-domain biology of Bcl-2-family members: IP3Rs and beyond.Contribution of oxidative stress to pathology in diaphragm and limb muscles with Duchenne muscular dystrophy.

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Calcium and the damage pathways in muscular dystrophy.

http://www.wikidata.org/entity/Q37710975

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 February 2010

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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

Calcium and the damage pathways in muscular dystrophy.

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Calcium and the damage pathways in muscular dystrophy.

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type

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Calcium and the damage pathways in muscular dystrophy.

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Calcium and the damage pathways in muscular dystrophy.

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prefLabel

Calcium and the damage pathways in muscular dystrophy.

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Calcium and the damage pathways in muscular dystrophy.

@nl

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Canadian Journal of Physiology and Pharmacology

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Calcium and the damage pathways in muscular dystrophy.

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David G Allen

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Ella W Yeung

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Nicholas P Whitehead

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Othon L Gervasio

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P2860

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Stretch-activated single ion channel currents in tissue-cultured embryonic chick skeletal muscle

Identification of a peptide toxin from Grammostola spatulata spider venom that blocks cation-selective stretch-activated channels

Mechanosensitive channel properties and membrane mechanics in mouse dystrophic myotubes

Cellular and molecular regulation of muscle regeneration

Changes in mechanosensitive channel gating following mechanical stimulation in skeletal muscle myotubes from the mdx mouse

Membrane organization of the dystrophin-glycoprotein complex

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

Duchenne dystrophy: electron microscopic findings pointing to a basic or early abnormality in the plasma membrane of the muscle fiber.

Excitation-contraction uncoupling: major role in contraction-induced muscle injury.

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83-91

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scholarly article

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10.1139/Y09-058

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2

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88

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2010-02-01T00:00:00Z

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20237582

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