LARGE can functionally bypass alpha-dystroglycan glycosylation defects in distinct congenital muscular dystrophies

Article Abstract:

Changes in the processing and function of alpha-dystroglycan (alpha-DG) resulting from the genetic manipulation of LARGE, the putative glycosyltransferase mutated both in LARGE (super myd) mice and in humans is investigated. The findings suggest that modulation of LARGE expression or activity is a viable therapeutic strategy for glycosyltransferase-deficient congenital muscular dystrophies.

United States, Gene mutations, Gene mutation

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Skipping to new therapies for muscular dystrophy

Article Abstract:

An approach that aims to correct RNA improves muscle function in a mouse model of a disease particularly recalcitrant to gene therapy. The distribution of postmitotic muscle fibers throughout the body and the individual packaging of each fiber in a dense sheath of connective tissue rendered unwilling recipients for exogenous genes.

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Gene delivery goes global

Article Abstract:

All of the skeletal muscles in the body must be transduced for the gene therapy of muscular dystrophies. The advantages of the approach, which permeabilizes the blood vessels using vascular endothelial growth factor (VEGF), are discussed.

Vascular endothelial growth factor

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