ArticleNature2013
LARGE glycans on dystroglycan function as a tunable matrix scaffold to prevent dystrophy.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
83 citing papers in PubMed, 131 citations in OpenAlex.
- Recent advances in the synthesis of α-dystroglycanRSC advances · 2026Review
- Five key challenges for the plasma membrane insertion of nicotinic acetylcholine receptors in cellular model systems.Molecular and cellular biochemistry · 2026Review
- Biosynthesis and Regulation of Laminin-Binding O-Mannosyl Glycans Related to Muscular Dystrophy.Advances in experimental medicine and biology · 2026Review
- Analysis of Dystrophin-Associated Glycoproteins: Focus on Expression and Glycosylation of Dystroglycan in Skeletal Muscle.Methods in molecular biology (Clifton, N.J.) · 2026Article
- 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
- Distinct functional domains of Dystroglycan regulate inhibitory synapse formation and maintenance in cerebellar Purkinje cells.Communications biology · 2025Article
- Malformations of Core M3 on α-Dystroglycan Are the Leading Cause of Dystroglycanopathies.Journal of molecular neuroscience : MN · 2025Review
- Sarcolemma resilience and skeletal muscle health require O-mannosylation of dystroglycan.Skeletal muscle · 2025Article
- Article
- Dystroglycan-HSPG interactions provide synaptic plasticity and specificity.Glycobiology · 2024Review
- Alternative Treatments to Exercise for the Attenuation of Disuse-Induced Skeletal Muscle Atrophy in Rats.Muscles (Basel, Switzerland) · 2024Article
- Deep Mutational Scanning in Disease-related Genes with Saturation Mutagenesis-Reinforced Functional Assays (SMuRF).bioRxiv : the preprint server for biology · 2024Article
- Matriglycan maintains t-tubule structural integrity in cardiac muscle.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Is developmental plasticity triggered by DNA methylation changes in the invasive cane toad (Ecology and evolution · 2024Article
- The underlying mechanisms of arenaviral entry through matriglycan.Frontiers in molecular biosciences · 2024Review
- Protein O-mannosylation: one sugar, several pathways, many functions.Glycobiology · 2023Review
- Identification of a short, single site matriglycan that maintains neuromuscular function in the mouse.bioRxiv : the preprint server for biology · 2023Article
- Article
23 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
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The dense glycan coat that surrounds every cell is essential for cellular development and physiological function, and it is becoming appreciated that its composition is highly dynamic. Post-translational addition of the polysaccharide repeating unit [-3-xylose-α1,3-glucuronic acid-β1-]n by like-acetylglucosaminyltransferase (LARGE) is required for the glycoprotein dystroglycan to function as a receptor for proteins in the extracellular matrix. Reductions in the amount of [-3-xylose-α1,3-glucuronic acid-β1-]n (hereafter referred to as LARGE-glycan) on dystroglycan result in heterogeneous forms of muscular dystrophy. However, neither patient nor mouse studies has revealed a clear correlation between glycosylation status and phenotype. This disparity can be attributed to our lack of knowledge of the cellular function of the LARGE-glycan repeat. Here we show that coordinated upregulation of Large and dystroglycan in differentiating mouse muscle facilitates rapid extension of LARGE-glycan repeat chains. Using synthesized LARGE-glycan repeats we show a direct correlation between LARGE-glycan extension and its binding capacity for extracellular matrix ligands. Blocking Large upregulation during muscle regeneration results in the synthesis of dystroglycan with minimal LARGE-glycan repeats in association with a less compact basement membrane, immature neuromuscular junctions and dysfunctional muscle predisposed to dystrophy. This was consistent with the finding that patients with increased clinical severity of disease have fewer LARGE-glycan repeats. Our results reveal that the LARGE-glycan of dystroglycan serves as a tunable extracellular matrix protein scaffold, the extension of which is required for normal skeletal muscle function.
Indexed as
Identifiers
What OpenQuestion holds
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.