ArticleNature chemical biology2016
Structural basis of laminin binding to the LARGE glycans on dystroglycan.
Article in Nature chemical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
78 citing papers in PubMed, 114 citations in OpenAlex.
- Roles and therapeutic prospects of the laminin family in disorders of the nervous system.Journal of translational medicine · 2026Review
- K48-ubiquitin-dependent proteases cut-up post-ER proteins.Nature communications · 2026Article
- Biosynthesis and Regulation of Laminin-Binding O-Mannosyl Glycans Related to Muscular Dystrophy.Advances in experimental medicine and biology · 2026Review
- Loss of cell-autonomously secreted laminin-α2 drives muscle stem cell dysfunction in LAMA2-related muscular dystrophy.Nature communications · 2025Article
- Alkyne-tagged ribitol-5-phosphate derivatives for metabolic labelling of alpha-dystroglycan.RSC chemical biology · 2025Article
- Xylose phosphatase activity of dystroglycan self-regulates its receptor function.bioRxiv : the preprint server for biology · 2025Article
- LARGE1 processively polymerizes length-controlled matriglycan on prodystroglycan.Nature communications · 2025Article
- Modeling glycans with AlphaFold 3: capabilities, caveats, and limitations.Glycobiology · 2025Article
- Defective O-mannosyl glycan synthesis in dystroglycanopathies: pathogenesis and therapeutic frontiers.Journal of human genetics · 2025Review
- Cryo-EM reveals molecular mechanisms underlying the inhibitory effect of netrin-4 on laminin matrix formation.Nature communications · 2025Article
- Distinct functional domains of Dystroglycan regulate inhibitory synapse formation and maintenance in cerebellar Purkinje cells.Communications biology · 2025Article
- Review
- Non-Integrin Laminin Receptors: Shedding New Light and Clarity on Their Involvement in Human Diseases.International journal of molecular sciences · 2025Review
- Review
- Ribitol and ribose treatments differentially affect metabolism of muscle tissue in FKRP mutant mice.Scientific reports · 2025Article
- The Link between Oxygen and Basement Membranes.Reviews of physiology, biochemistry and pharmacology · 2025Review
- Article
- Identifying therapeutic targets for kidney stone disease through proteome-wide Mendelian randomization and colocalization analysis.Urolithiasis · 2024Article
- Validation of a novel western blot assay to monitor patterns and levels of alpha dystroglycan in skeletal muscle of patients with limb girdle muscular dystrophies.Journal of muscle research and cell motility · 2024Article
- Dystroglycan-HSPG interactions provide synaptic plasticity and specificity.Glycobiology · 2024Review
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Dystroglycan is a highly glycosylated extracellular matrix receptor with essential functions in skeletal muscle and the nervous system. Reduced matrix binding by α-dystroglycan (α-DG) due to perturbed glycosylation is a pathological feature of several forms of muscular dystrophy. Like-acetylglucosaminyltransferase (LARGE) synthesizes the matrix-binding heteropolysaccharide [-glucuronic acid-β1,3-xylose-α1,3-]n. Using a dual exoglycosidase digestion, we confirm that this polysaccharide is present on native α-DG from skeletal muscle. The atomic details of matrix binding were revealed by a high-resolution crystal structure of laminin-G-like (LG) domains 4 and 5 (LG4 and LG5) of laminin-α2 bound to a LARGE-synthesized oligosaccharide. A single glucuronic acid-β1,3-xylose disaccharide repeat straddles a Ca(2+) ion in the LG4 domain, with oxygen atoms from both sugars replacing Ca(2+)-bound water molecules. The chelating binding mode accounts for the high affinity of this protein-carbohydrate interaction. These results reveal a previously uncharacterized mechanism of carbohydrate recognition and provide a structural framework for elucidating the mechanisms underlying muscular dystrophy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.