Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle. - Wikidata - awgldk - TriplyDB

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

http://www.wikidata.org/entity/Q34627089

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Molecular and cell-based therapies for muscle degenerations: a road under construction Tropomodulin capping of actin filaments in striated muscle development and physiology Dysferlin at transverse tubules regulates Ca(2+) homeostasis in skeletal muscle 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 A micropeptide encoded by a putative long noncoding RNA regulates muscle performance Pregnancy-induced amelioration of muscular dystrophy phenotype in mdx mice via muscle membrane stabilization effect of glucocorticoid SEPN1, an endoplasmic reticulum-localized selenoprotein linked to skeletal muscle pathology, counteracts hyperoxidation by means of redox-regulating SERCA2 pump activity Hsp72 preserves muscle function and slows progression of severe muscular dystrophy Enhancing muscle membrane repair by gene delivery of MG53 ameliorates muscular dystrophy and heart failure in δ-Sarcoglycan-deficient hamsters.Muscle lipogenesis balances insulin sensitivity and strength through calcium signaling.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.P38α MAPK underlies muscular dystrophy and myofiber death through a Bax-dependent mechanism.High-throughput FRET assay yields allosteric SERCA activators Orai1 mediates exacerbated Ca(2+) entry in dystrophic skeletal muscle Perturbations in intracellular Ca2+ handling in skeletal muscle in the G93A*SOD1 mouse model of amyotrophic lateral sclerosis.The FVB Background Does Not Dramatically Alter the Dystrophic Phenotype of Mdx Mice SERCA2a gene transfer improves electrocardiographic performance in aged mdx mice Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Triadopathies: an emerging class of skeletal muscle diseases.SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models.Adaptive strength gains in dystrophic muscle exposed to repeated bouts of eccentric contraction Duchenne muscular dystrophy gene therapy in the canine model.Signs of progress in gene therapy for muscular dystrophy also warrant caution 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 Lipogenesis mitigates dysregulated sarcoplasmic reticulum calcium uptake in muscular dystrophy.Nanospan, an alternatively spliced isoform of sarcospan, localizes to the sarcoplasmic reticulum in skeletal muscle and is absent in limb girdle muscular dystrophy 2F.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Skeletal Muscle Phospholipid Metabolism Regulates Insulin Sensitivity and Contractile Function.Calpain 3 deficiency affects SERCA expression and function in the skeletal muscle.Interactions between sarco-endoplasmic reticulum and mitochondria in cardiac and skeletal muscle - pivotal roles in Ca²⁺ and reactive oxygen species signaling.Ca²⁺-pumping impairment during repetitive fatiguing contractions in single myofibers: role of cross-bridge cycling.Thrombospondin expression in myofibers stabilizes muscle membranes.Mitochondrial alterations and oxidative stress in an acute transient mouse model of muscle degeneration: implications for muscular dystrophy and related muscle pathologies.Hyperactive adverse mechanical stress responses in dystrophic heart are coupled to transient receptor potential canonical 6 and blocked by cGMP-protein kinase G modulation.Cell-matrix interactions in muscle disease.Update on the treatment of Duchenne muscular dystrophy.

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Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

http://www.wikidata.org/entity/Q34627089

description

2011 nî lūn-bûn

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2011 թուականի Մարտին հրատարակուած գիտական յօդուած

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2011 թվականի մարտին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@ast

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@en

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@nl

type

label

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@ast

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@en

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@nl

prefLabel

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@ast

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@en

Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@nl

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Journal of Clinical Investigation

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Mitigation of muscular dystrophy in mice by SERCA overexpression in skeletal muscle.

@en

P2093

Chi K Lam

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Douglas P Millay

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Evangelia G Kranias

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Michelle A Sargent

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Roger J Hajjar

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Sanjeewa A Goonasekera

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P2860

Leaky RyR2 trigger ventricular arrhythmias in Duchenne muscular dystrophy

Hypernitrosylated ryanodine receptor calcium release channels are leaky in dystrophic muscle

Prevention of cardiomyopathy in mouse models lacking the smooth muscle sarcoglycan-sarcospan complex

Chronic administration of membrane sealant prevents severe cardiac injury and ventricular dilatation in dystrophic dogs.

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

Sarcoplasmic reticulum: the dynamic calcium governor of muscle.

The role of Ca2+ in muscle cell damage.

Muscle damage in mdx (dystrophic) mice: role of calcium and reactive oxygen species.

Increased calcium influx in dystrophic muscle.

Pathophysiology of duchenne muscular dystrophy: current hypotheses.

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1044-1052

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10.1172/JCI43844

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3

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121

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Jeffery D. Molkentin

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2011-03-01T00:00:00Z

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49802412

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21285509

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3049367

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