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Mutations in B3GALNT2 cause congenital muscular dystrophy and hypoglycosylation of a-dystroglycan.
LARGE can functionally bypass alpha-dystroglycan glycosylation defects in distinct congenital muscular dystrophies.
Molecular recognition by LARGE is essential for expression of functional dystroglycan.
O-mannosyl phosphorylation of alpha-dystroglycan is required for laminin binding.
Post-translational disruption of dystroglycan-ligand interactions in congenital muscular dystrophies.
Disruption of perlecan binding and matrix assembly by post-translational or genetic disruption of dystroglycan function.
Functional glycosylation of dystroglycan is crucial for thymocyte development in the mouse.
Like-acetylglucosaminyltransferase (LARGE)-dependent modification of dystroglycan at Thr-317/319 is required for laminin binding and arenavirus infection.
Basal lamina strengthens cell membrane integrity via the laminin G domain-binding motif of alpha-dystroglycan.
Mouse fukutin deletion impairs dystroglycan processing and recapitulates muscular dystrophy.
Residual laminin-binding activity and enhanced dystroglycan glycosylation by LARGE in novel model mice to dystroglycanopathy.
Dystroglycan: from biosynthesis to pathogenesis of human disease.
Old World arenavirus infection interferes with the expression of functional alpha-dystroglycan in the host cell.
The glucuronyltransferase B4GAT1 is required for initiation of LARGE-mediated a-dystroglycan functional glycosylation.