ArticleThe Journal of biological chemistry2011
Glycomic analyses of mouse models of congenital muscular dystrophy.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 81 citations in OpenAlex.
- Branching of O-mannose glycans regulates node of Ranvier organization and saltatory conduction.Communications biology · 2026Article
- Defining substrate specificities ofOrganic chemistry frontiers : an international journal of organic chemistry · 2026Article
- Expression of Dystroglycanopathy-Related Enzymes, POMGNT2 and POMGNT1, in the Mammalian Retina and 661W Cone-like Cell Line.Biomedicines · 2025Article
- Sarcolemma resilience and skeletal muscle health require O-mannosylation of dystroglycan.Skeletal muscle · 2025Article
- Global View of Domain-Specific O-Linked Mannose Glycosylation in Glycoengineered Cells.Molecular & cellular proteomics : MCP · 2024Article
- Protein O-mannosylation: one sugar, several pathways, many functions.Glycobiology · 2023Review
- Rhinovirus induces airway remodeling: what are the physiological consequences?Respiratory research · 2023Review
- Exploring the In situ pairing of human galectins toward synthetic O-mannosylated core M1 glycopeptides of α-dystroglycan.Scientific reports · 2022Article
- Mammalian brain glycoproteins exhibit diminished glycan complexity compared to other tissues.Nature communications · 2022Article
- Contrasting the conformational effects of α-O-GalNAc and α-O-Man glycan protein modifications and their impact on the mucin-like region of alpha-dystroglycan.Glycobiology · 2021Article
- Separation and Identification of Permethylated Glycan Isomers by Reversed Phase NanoLC-NSI-MSMolecular & cellular proteomics : MCP · 2021Article
- biAb Mediated Restoration of the Linkage between Dystroglycan and Laminin-211 as a Therapeutic Approach for α-Dystroglycanopathies.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- 3D Structure and Function of Glycosyltransferases Involved inInternational journal of molecular sciences · 2020Review
- Remarkable Homeostasis of Protein Sialylation in Skeletal Muscles of Hibernating Daurian Ground Squirrels (Frontiers in physiology · 2020Article
- Laminin G-like domains: dystroglycan-specific lectins.Current opinion in structural biology · 2019Review
- Facile Chemoenzymatic Synthesis of O-Mannosyl Glycans.Angewandte Chemie (International ed. in English) · 2018Article
- Towards automation of glycomic profiling of complex biological materials.Glycoconjugate journal · 2018Article
- Recent advancements in understanding mammalian O-mannosylation.Glycobiology · 2017Review
- Whoa man! Unexpected proteinThe Journal of biological chemistry · 2017Review
- Carbohydrate-binding domain of the POMGnT1 stem region modulates O-mannosylation sites of α-dystroglycan.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Dystroglycanopathies are a subset of congenital muscular dystrophies wherein α-dystroglycan (α-DG) is hypoglycosylated. α-DG is an extensively O-glycosylated extracellular matrix-binding protein and a key component of the dystrophin-glycoprotein complex. Previous studies have shown α-DG to be post-translationally modified by both O-GalNAc- and O-mannose-initiated glycan structures. Mutations in defined or putative glycosyltransferase genes involved in O-mannosylation are associated with a loss of ligand-binding activity of α-DG and are causal for various forms of congenital muscular dystrophy. In this study, we sought to perform glycomic analysis on brain O-linked glycan structures released from proteins of three different knock-out mouse models associated with O-mannosylation (POMGnT1, LARGE (Myd), and DAG1(-/-)). Using mass spectrometry approaches, we were able to identify nine O-mannose-initiated and 25 O-GalNAc-initiated glycan structures in wild-type littermate control mouse brains. Through our analysis, we were able to confirm that POMGnT1 is essential for the extension of all observed O-mannose glycan structures with β1,2-linked GlcNAc. Loss of LARGE expression in the Myd mouse had no observable effect on the O-mannose-initiated glycan structures characterized here. Interestingly, we also determined that similar amounts of O-mannose-initiated glycan structures are present on brain proteins from α-DG-lacking mice (DAG1) compared with wild-type mice, indicating that there must be additional proteins that are O-mannosylated in the mammalian brain. Our findings illustrate that classical β1,2-elongation and β1,6-GlcNAc branching of O-mannose glycan structures are dependent upon the POMGnT1 enzyme and that O-mannosylation is not limited solely to α-DG in the brain.
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.