Neuromuscular disease. DOK7 gene therapy benefits mouse models of diseases characterized by defects in the neuromuscular junction.
about
Pathogenesis of myasthenia gravis: update on disease types, models, and mechanismsScalable downstream strategies for purification of recombinant adeno- associated virus vectors in light of the properties.Dietary milk fat globule membrane supplementation combined with regular exercise improves skeletal muscle strength in healthy adults: a randomized double-blind, placebo-controlled, crossover trial.Nonmechanical Roles of Dystrophin and Associated Proteins in Exercise, Neuromuscular Junctions, and Brains.Lentivirus-mediated Persephin over-expression in Parkinson's disease ratsSorbs1 and -2 Interact with CrkL and Are Required for Acetylcholine Receptor Cluster Formation.Forced expression of muscle specific kinase slows postsynaptic acetylcholine receptor loss in a mouse model of MuSK myasthenia gravisEnhancing Transgene Expression from Recombinant AAV8 Vectors in Different Tissues Using Woodchuck Hepatitis Virus Post-Transcriptional Regulatory ElementNeuromuscular junction degeneration in muscle wasting.Recombinant adeno-associated virus vectors in the treatment of rare diseases.DOK7 gene therapy enhances motor activity and life span in ALS model mice.Postnatal knockdown of dok-7 gene expression in mice causes structural defects in neuromuscular synapses and myasthenic pathology.Gene therapy: Going from strength to strength.Cardiac troponin T and fast skeletal muscle denervation in ageing.Clinical and research strategies for limb-girdle congenital myasthenic syndromes.The mouse passive-transfer model of MuSK myasthenia gravis: disrupted MuSK signaling causes synapse failure.Preserving neuromuscular synapses in ALS by stimulating MuSK with a therapeutic agonist antibody.Fundamental Molecules and Mechanisms for Forming and Maintaining Neuromuscular Synapses.The carboxyl-terminal region of Dok-7 plays a key, but not essential, role in activation of muscle-specific receptor kinase MuSK and neuromuscular synapse formation.Treating pediatric neuromuscular disorders: The future is now.The beta-adrenergic agonist salbutamol modulates neuromuscular junction formation in zebrafish models of human myasthenic syndromes.Animal Models of the Neuromuscular Junction, Vitally Informative for Understanding Function and the Molecular Mechanisms of Congenital Myasthenic Syndromes.
P2860
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P2860
Neuromuscular disease. DOK7 gene therapy benefits mouse models of diseases characterized by defects in the neuromuscular junction.
description
2014 nî lūn-bûn
@nan
2014年の論文
@ja
2014年論文
@yue
2014年論文
@zh-hant
2014年論文
@zh-hk
2014年論文
@zh-mo
2014年論文
@zh-tw
2014年论文
@wuu
2014年论文
@zh
2014年论文
@zh-cn
name
Neuromuscular disease. DOK7 ge ...... in the neuromuscular junction.
@en
Neuromuscular disease. DOK7 ge ...... in the neuromuscular junction.
@nl
type
label
Neuromuscular disease. DOK7 ge ...... in the neuromuscular junction.
@en
Neuromuscular disease. DOK7 ge ...... in the neuromuscular junction.
@nl
prefLabel
Neuromuscular disease. DOK7 ge ...... in the neuromuscular junction.
@en
Neuromuscular disease. DOK7 ge ...... in the neuromuscular junction.
@nl
P2093
P2860
P356
P1433
P1476
Neuromuscular disease. DOK7 ge ...... in the neuromuscular junction.
@en
P2093
David Beeson
Masakatsu Motomura
Nobuaki Yoshida
Shin'ichi Takeda
Sumimasa Arimura
Takashi Okada
Tohru Tezuka
Tomoko Chiyo
Toshiro Yoshimura
Yuji Yamanashi
P2860
P304
P356
10.1126/SCIENCE.1250744
P407
P577
2014-09-01T00:00:00Z