An agrin minigene rescues dystrophic symptoms in a mouse model for congenital muscular dystrophy.
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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 miceDevelopmental and pathogenic mechanisms of basement membrane assemblyDistinct roles for laminin globular domains in laminin alpha1 chain mediated rescue of murine laminin alpha2 chain deficiencyHanging on for the ride: adhesion to the extracellular matrix mediates cellular responses in skeletal muscle morphogenesis and diseaseInhibition of synapse assembly in mammalian muscle in vivo by RNA interferenceRole of laminin terminal globular domains in basement membrane assemblyMuscle-wide secretion of a miniaturized form of neural agrin rescues focal neuromuscular innervation in agrin mutant mice.NAD+ biosynthesis ameliorates a zebrafish model of muscular dystrophy.Laminin alpha1 chain mediated reduction of laminin alpha2 chain deficient muscular dystrophy involves integrin alpha7beta1 and dystroglycan.Duplication of the dystroglycan gene in most branches of teleost fish.Improving Reproducibility of Phenotypic Assessments in the DyW Mouse Model of Laminin-α2 Related Congenital Muscular Dystrophy.Amelioration of laminin-alpha2-deficient congenital muscular dystrophy by somatic gene transfer of miniagrin.Overexpression of the cytotoxic T cell GalNAc transferase in skeletal muscle inhibits muscular dystrophy in mdx miceLRP4 is critical for neuromuscular junction maintenanceThe heparan sulfate proteoglycan agrin contributes to barrier properties of mouse brain endothelial cells by stabilizing adherens junctions.Basement membranes: cell scaffoldings and signaling platforms.Muscle-specific expression of insulin-like growth factor 1 improves outcome in Lama2Dy-w mice, a model for congenital muscular dystrophy type 1APeripheral nerve pathology, including aberrant Schwann cell differentiation, is ameliorated by doxycycline in a laminin-α2-deficient mouse model of congenital muscular dystrophy.Transgenic overexpression of dystroglycan does not inhibit muscular dystrophy in mdx miceTransgenic expression of {alpha}7{beta}1 integrin maintains muscle integrity, increases regenerative capacity, promotes hypertrophy, and reduces cardiomyopathy in dystrophic mice.Elimination of myostatin does not combat muscular dystrophy in dy mice but increases postnatal lethality.Quantitative proteomic analysis reveals metabolic alterations, calcium dysregulation, and increased expression of extracellular matrix proteins in laminin α2 chain-deficient muscle.Proinflammatory signals and the loss of lymphatic vessel hyaluronan receptor-1 (LYVE-1) in the early pathogenesis of laminin alpha2-deficient skeletal muscle.An immunological analysis of dystroglycan subunits: lessons learned from a small cohort of non-congenital dystrophic patients.ADAM12 alleviates the skeletal muscle pathology in mdx dystrophic mice.Disruption of glomerular basement membrane charge through podocyte-specific mutation of agrin does not alter glomerular permselectivityOverexpression 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 stagesCoordinate control of axon defasciculation and myelination by laminin-2 and -8.Role of extracellular matrix proteins and their receptors in the development of the vertebrate neuromuscular junctionSchwann cell myelination requires integration of laminin activities.Laminin-211 in skeletal muscle function.Laminins in basement membrane assemblyThe congenital muscular dystrophies: recent advances and molecular insights.EvoDesign: De novo protein design based on structural and evolutionary profiles.Pathology is alleviated by doxycycline in a laminin-alpha2-null model of congenital muscular dystrophyScaffold-forming and Adhesive Contributions of Synthetic Laminin-binding Proteins to Basement Membrane AssemblyOverexpression of Galgt2 reduces dystrophic pathology in the skeletal muscles of alpha sarcoglycan-deficient mice
P2860
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P2860
An agrin minigene rescues dystrophic symptoms in a mouse model for congenital muscular dystrophy.
description
2001 nî lūn-bûn
@nan
2001 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@ast
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@en
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@nl
type
label
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@ast
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@en
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@nl
prefLabel
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@ast
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@en
An agrin minigene rescues dyst ...... congenital muscular dystrophy.
@nl
P2093
P356
P1433
P1476
An agrin minigene rescues dyst ...... congenital muscular dystrophy
@en
P2093
Barzaghi P
Bezakova G
P2888
P304
P356
10.1038/35095054
P407
P577
2001-09-01T00:00:00Z
P6179
1040563474