ArticleeLife2014
The glucuronyltransferase B4GAT1 is required for initiation of LARGE-mediated α-dystroglycan functional glycosylation.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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.
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.
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Who cites it
75 citing papers in PubMed, 128 citations in OpenAlex.
- Article
- [Association between umbilical cord blood proteome and early infant neurodevelopmental risk].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2026Article
- Longitudinal analysis of human milk oligosaccharides and mucin-2-glycans in infants reveals enrichment of sulfated and glucuronic acid-bearing HMOs.The Journal of biological chemistry · 2026Article
- Article
- Recent advances in the synthesis of α-dystroglycanRSC advances · 2026Review
- Biosynthesis and Regulation of Laminin-Binding O-Mannosyl Glycans Related to Muscular Dystrophy.Advances in experimental medicine and biology · 2026Review
- Expression of Dystroglycanopathy-Related Enzymes, POMGNT2 and POMGNT1, in the Mammalian Retina and 661W Cone-like Cell Line.Biomedicines · 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
- Heterogeneity of Extracellular Vesicles and Non-Vesicular Nanoparticles in Glioblastoma.Journal of extracellular vesicles · 2025Article
- Defective O-mannosyl glycan synthesis in dystroglycanopathies: pathogenesis and therapeutic frontiers.Journal of human genetics · 2025Review
- UDP-glucose dehydrogenase variants cause dystroglycanopathy.Annals of clinical and translational neurology · 2025Article
- Review
- Long-term CSF responses in adult patients with spinal muscular atrophy type 2 or 3 on treatment with nusinersen.Journal of neurology · 2025Article
- Ribitol and ribose treatments differentially affect metabolism of muscle tissue in FKRP mutant mice.Scientific reports · 2025Article
- Article
- Article
- Molecular signatures of normal pressure hydrocephalus: a large-scale proteomic analysis of cerebrospinal fluid.Fluids and barriers of the CNS · 2024Article
- Deep Mutational Scanning in Disease-related Genes with Saturation Mutagenesis-Reinforced Functional Assays (SMuRF).bioRxiv : the preprint server for biology · 2024Article
- Article
15 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 2 countries.
Funding
Abstract
Dystroglycan is a cell membrane receptor that organizes the basement membrane by binding ligands in the extracellular matrix. Proper glycosylation of the α-dystroglycan (α-DG) subunit is essential for these activities, and lack thereof results in neuromuscular disease. Currently, neither the glycan synthesis pathway nor the roles of many known or putative glycosyltransferases that are essential for this process are well understood. Here we show that FKRP, FKTN, TMEM5 and B4GAT1 (formerly known as B3GNT1) localize to the Golgi and contribute to the O-mannosyl post-phosphorylation modification of α-DG. Moreover, we assigned B4GAT1 a function as a xylose β1,4-glucuronyltransferase. Nuclear magnetic resonance studies confirmed that a glucuronic acid β1,4-xylose disaccharide synthesized by B4GAT1 acts as an acceptor primer that can be elongated by LARGE with the ligand-binding heteropolysaccharide. Our findings greatly broaden the understanding of α-DG glycosylation and provide mechanistic insight into why mutations in B4GAT1 disrupt dystroglycan function and cause disease.
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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.