Amelioration of laminin-alpha2-deficient congenital muscular dystrophy by somatic gene transfer of miniagrin. - sprookjes - yvandenbroek - TriplyDB

Amelioration of laminin-alpha2-deficient congenital muscular dystrophy by somatic gene transfer of miniagrin.

Amelioration of laminin-alpha2-deficient congenital muscular dystrophy by somatic gene transfer of miniagrin.

http://www.wikidata.org/entity/Q33922811

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Skeletal muscle laminin and MDC1A: pathogenesis and treatment strategies.Apoptosis inhibitors and mini-agrin have additive benefits in congenital muscular dystrophy mice Developmental and pathogenic mechanisms of basement membrane assembly Distinct roles for laminin globular domains in laminin alpha1 chain mediated rescue of murine laminin alpha2 chain deficiency AAV-mediated intramuscular delivery of myotubularin corrects the myotubular myopathy phenotype in targeted murine muscle and suggests a function in plasma membrane homeostasis Efficacy of Gene Therapy Is Dependent on Disease Progression in Dystrophic Mice with Mutations in the FKRP Gene Efficient retrograde transport of adeno-associated virus type 8 to spinal cord and dorsal root ganglion after vector delivery in muscle.Post-Natal knockdown of fukutin-related protein expression in muscle by long-termRNA interference induces dystrophic pathology [corrected]Proinflammatory signals and the loss of lymphatic vessel hyaluronan receptor-1 (LYVE-1) in the early pathogenesis of laminin alpha2-deficient skeletal muscle.AAV-8 is more efficient than AAV-9 in transducing neonatal dog heart.Signs of progress in gene therapy for muscular dystrophy also warrant caution Overexpression of the cytotoxic T cell (CT) carbohydrate inhibits muscular dystrophy in the dyW mouse model of congenital muscular dystrophy 1A.Mesoangioblast delivery of miniagrin ameliorates murine model of merosin-deficient congenital muscular dystrophy type 1A.Linker molecules between laminins and dystroglycan ameliorate laminin-alpha2-deficient muscular dystrophy at all disease stages Liver-specific microRNA-122 target sequences incorporated in AAV vectors efficiently inhibits transgene expression in the liver.Efficient whole-body transduction with trans-splicing adeno-associated viral vectors Prospect of gene therapy for cardiomyopathy in hereditary muscular dystrophy.Scaffold-forming and Adhesive Contributions of Synthetic Laminin-binding Proteins to Basement Membrane Assembly Overexpression of Galgt2 reduces dystrophic pathology in the skeletal muscles of alpha sarcoglycan-deficient mice K137R mutation on adeno-associated viral capsids had minimal effect on enhancing gene delivery in vivo.Congenital muscular dystrophy. Part II: a review of pathogenesis and therapeutic perspectives.AAV-directed muscular dystrophy gene therapy.Cell-matrix interactions in muscle disease.Laminin: loss-of-function studies.Chimeric protein repair of laminin polymerization ameliorates muscular dystrophy phenotype.Angiotensin II type 1 receptor antagonists alleviate muscle pathology in the mouse model for laminin-α2-deficient congenital muscular dystrophy (MDC1A).Hydrodynamic limb vein injection of adeno-associated virus serotype 8 vector carrying canine myostatin propeptide gene into normal dogs enhances muscle growth.Follistatin N terminus differentially regulates muscle size and fat in vivo.Laminin alpha1 chain improves laminin alpha2 chain deficient peripheral neuropathy.Muscle and heart function restoration in a limb girdle muscular dystrophy 2I (LGMD2I) mouse model by systemic FKRP gene delivery.Protein trans-splicing as a means for viral vector-mediated in vivo gene therapy.ECM-Related Myopathies and Muscular Dystrophies: Pros and Cons of Protein Therapies.Linker proteins restore basement membrane and correct LAMA2-related muscular dystrophy in mice.Laminin-deficient muscular dystrophy: Molecular pathogenesis and structural repair strategies.Muscular dystrophy meets protein biochemistry, the mother of invention.Amelioration of Muscle and Nerve Pathology in LAMA2 Muscular Dystrophy by AAV9-Mini-Agrin.Proteasome inhibition improves the muscle of laminin α2 chain-deficient mice.At the Crossroads of Clinical and Preclinical Research for Muscular Dystrophy-Are We Closer to Effective Treatment for Patients?

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Amelioration of laminin-alpha2-deficient congenital muscular dystrophy by somatic gene transfer of miniagrin.

http://www.wikidata.org/entity/Q33922811

description

2005 nî lūn-bûn

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Amelioration of laminin-alpha2 ...... ic gene transfer of miniagrin.

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Amelioration of laminin-alpha2 ...... ic gene transfer of miniagrin.

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Amelioration of laminin-alpha2 ...... ic gene transfer of miniagrin.

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Amelioration of laminin-alpha2 ...... ic gene transfer of miniagrin.

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Amelioration of laminin-alpha2 ...... ic gene transfer of miniagrin.

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

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Amelioration of laminin-alpha2 ...... ic gene transfer of miniagrin.

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Chunlian Chen

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Chunping Qiao

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Jianbin Li

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Juan Li

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Romesh Draviam

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Simon Watkins

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Tong Zhu

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Xiao Xiao

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Xiaojing Ye

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P2860

Form and function: the laminin family of heterotrimers

Agrin is a high-affinity binding protein of dystroglycan in non-muscle tissue

An ancient retrotransposal insertion causes Fukuyama-type congenital muscular dystrophy

Production of high-titer recombinant adeno-associated virus vectors in the absence of helper adenovirus

Novel adeno-associated viruses from rhesus monkeys as vectors for human gene therapy

Assignment of the muscle-eye-brain disease gene to 1p32-p34 by linkage analysis and homozygosity mapping.

The dystroglycan complex is necessary for stabilization of acetylcholine receptor clusters at neuromuscular junctions and formation of the synaptic basement membrane

A novel laminin alpha2 isoform in severe laminin alpha2 deficient congenital muscular dystrophy

rAAV vector-mediated sarcogylcan gene transfer in a hamster model for limb girdle muscular dystrophy

Dystroglycan-alpha, a dystrophin-associated glycoprotein, is a functional agrin receptor

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10.1073/PNAS.0502137102

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16103356

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