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Article

Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin-like growth factor 1 and aggravates muscular dystrophy in mice.

Human molecular genetics - 1 Sept 2014

Saito Fumiaki, Kanagawa Motoi, Ikeda Miki, Hagiwara Hiroki, Masaki Toshihiro, Ohkuma Hidehiko, Katanosaka Yuki, Shimizu Teruo, Sonoo Masahiro, Toda Tatsushi, Matsumura Kiichiro

Abstract excerpt

Several types of muscular dystrophy are caused by defective linkage between α-dystroglycan (α-DG) and laminin. Among these, dystroglycanopathy, including Fukuyama-type congenital muscular dystrophy (FCMD), results from abnormal glycosylation of α-DG. Recent studies have shown that like-acetylglucosaminyltransferase (LARGE) strongly enhances the laminin-binding activity of α-DG. Therefore, restoration of the...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 24722207
DOI: 10.1093/hmg/ddu168

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Related research

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Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin-like growth factor 1 and aggravates muscular dystrophy in mice.PMID 24722207Read ↗

Fukutin is prerequisite to ameliorate muscular dystrophic phenotype by myofiber-selective LARGE expressionSemantic proximity Read ↗

The transgenic expression of LARGE exacerbates the muscle phenotype of dystroglycanopathy mice.Semantic proximity Read ↗

Adeno-associated virus-mediated overexpression of LARGE rescues α-dystroglycan function in dystrophic mice with mutations in the fukutin-related protein.Semantic proximity Read ↗

Laminin alpha1 chain reduces muscular dystrophy in laminin alpha2 chain deficient mice.Semantic proximity Read ↗

<i>Large1</i> Gene Transfer in Older <i>myd</i> Mice with Severe Muscular Dystrophy Restores Muscle Function and Greatly Improves SurvivalSemantic proximity Read ↗

Muscle-specific expression of insulin-like growth factor 1 improves outcome in Lama2Dy-w mice, a model for congenital muscular dystrophy type 1ASemantic proximity Read ↗

Autophagy is increased in laminin α2 chain-deficient muscle and its inhibition improves muscle morphology in a mouse model of MDC1A.Semantic proximity Read ↗

Laminin-α2 Chain-Deficient Congenital Muscular Dystrophy: Pathophysiology and Development of Treatment.Semantic proximity Read ↗

Investigating the functions of LARGE: lessons from mutant mice.Semantic proximity Read ↗

Transgenic Overexpression of LARGE Induces α-Dystroglycan Hyperglycosylation in Skeletal and Cardiac MuscleSemantic proximity Read ↗

Muscle-specific expression of LARGE restores neuromuscular transmission deficits in dystrophic LARGEmyd miceSemantic proximity Read ↗

Adeno-associated viral-mediated LARGE gene therapy rescues the muscular dystrophic phenotype in mouse models of dystroglycanopathy.Semantic proximity Read ↗

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