Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism. - Wikidata - awgldk - TriplyDB

Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism.

Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism.

http://www.wikidata.org/entity/Q37419160

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Leaky RyR2 trigger ventricular arrhythmias in Duchenne muscular dystrophy Pre-clinical drug tests in the mdx mouse as a model of dystrophinopathies: an overview Dysferlin at transverse tubules regulates Ca(2+) homeostasis in skeletal muscle Early pathogenesis of Duchenne muscular dystrophy modelled in patient-derived human induced pluripotent stem cells.MicroRNA-3906 regulates fast muscle differentiation through modulating the target gene homer-1b in zebrafish embryos Interaction between mitsugumin 29 and TRPC3 participates in regulating Ca(2+) transients in skeletal muscle Anti-inflammatory drugs for Duchenne muscular dystrophy: focus on skeletal muscle-releasing factors Current understanding of molecular pathology and treatment of cardiomyopathy in duchenne muscular dystrophy Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy Apoptosis repressor with a CARD domain (ARC) restrains Bax-mediated pathogenesis in dystrophic skeletal muscle Metformin protects skeletal muscle from cardiotoxin induced degeneration Constitutive activation of the calcium sensor STIM1 causes tubular-aggregate myopathy Enhancing muscle membrane repair by gene delivery of MG53 ameliorates muscular dystrophy and heart failure in δ-Sarcoglycan-deficient hamsters.Microtubules underlie dysfunction in duchenne muscular dystrophy.Functional KCa1.1 channels are crucial for regulating the proliferation, migration and differentiation of human primary skeletal myoblasts Transcriptional response of zebrafish embryos exposed to neurotoxic compounds reveals a muscle activity dependent hspb11 expression.Dystrophic Cardiomyopathy-Potential Role of Calcium in Pathogenesis, Treatment and Novel Therapies Enhanced Ca²⁺ influx from STIM1-Orai1 induces muscle pathology in mouse models of muscular dystrophy.Absence of γ-sarcoglycan alters the response of p70S6 kinase to mechanical perturbation in murine skeletal muscle.Mechanisms of muscle weakness in muscular dystrophy TRPC3 cation channel plays an important role in proliferation and differentiation of skeletal muscle myoblasts.P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.Long-term blocking of calcium channels in mdx mice results in differential effects on heart and skeletal muscle Orai1 mediates exacerbated Ca(2+) entry in dystrophic skeletal muscle Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.Loss of nNOS inhibits compensatory muscle hypertrophy and exacerbates inflammation and eccentric contraction-induced damage in mdx mice.Electroporation as a method to induce myofiber regeneration and increase the engraftment of myogenic cells in skeletal muscles of primates.Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Effects of steroids and angiotensin converting enzyme inhibition on circumferential strain in boys with Duchenne muscular dystrophy: a cross-sectional and longitudinal study utilizing cardiovascular magnetic resonance.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.Phospholamban overexpression in mice causes a centronuclear myopathy-like phenotype.Increased resting intracellular calcium modulates NF-κB-dependent inducible nitric-oxide synthase gene expression in dystrophic mdx skeletal myotubes Cavin4b/Murcb Is Required for Skeletal Muscle Development and Function in Zebrafish.Temperature and RyR1 regulate the activation rate of store-operated Ca²+ entry current in myotubes Membrane Repair: Mechanisms and Pathophysiology.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Defects in mitochondrial localization and ATP synthesis in the mdx mouse model of Duchenne muscular dystrophy are not alleviated by PDE5 inhibition Genetic overexpression of Serpina3n attenuates muscular dystrophy in mice.Cardiac phenotype of Duchenne Muscular Dystrophy: insights from cellular studies

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Calcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism.

http://www.wikidata.org/entity/Q37419160

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 28 October 2009

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

Calcium influx is sufficient t ...... gh a TRPC-dependent mechanism.

@en

Calcium influx is sufficient t ...... gh a TRPC-dependent mechanism.

@nl

type

label

Calcium influx is sufficient t ...... gh a TRPC-dependent mechanism.

@en

Calcium influx is sufficient t ...... gh a TRPC-dependent mechanism.

@nl

prefLabel

Calcium influx is sufficient t ...... gh a TRPC-dependent mechanism.

@en

Calcium influx is sufficient t ...... gh a TRPC-dependent mechanism.

@nl

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PNAS.0906591106

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Proceedings of the National Academy of Sciences of the United States of America

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Calcium influx is sufficient t ...... gh a TRPC-dependent mechanism.

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Douglas P Millay

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Marjorie Maillet

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Michelle A Sargent

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Sanjeewa A Goonasekera

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P2860

Subunit composition of mammalian transient receptor potential channels in living cells

Defective membrane repair in dysferlin-deficient muscular dystrophy

Dysferlin, a novel skeletal muscle gene, is mutated in Miyoshi myopathy and limb girdle muscular dystrophy

A gene related to Caenorhabditis elegans spermatogenesis factor fer-1 is mutated in limb-girdle muscular dystrophy type 2B

Impaired neuromuscular transmission and skeletal muscle fiber necrosis in mice lacking Na/Ca exchanger 3

Function and genetics of dystrophin and dystrophin-related proteins in muscle.

Calcium-dependent facilitation and graded deactivation of store-operated calcium entry in fetal skeletal muscle

The dystrophin glycoprotein complex: signaling strength and integrity for the sarcolemma.

Muscular dystrophies involving the dystrophin-glycoprotein complex: an overview of current mouse models.

Elevated subsarcolemmal Ca2+ in mdx mouse skeletal muscle fibers detected with Ca2+-activated K+ channels.

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19023-19028

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scholarly article

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10.1073/PNAS.0906591106

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Jeffery D. Molkentin

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2009-10-28T00:00:00Z

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38043693

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19864620

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2776441

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