ArticleGlycobiology2012
Differential glycosylation of α-dystroglycan and proteins other than α-dystroglycan by like-glycosyltransferase.
Article in Glycobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 29 citations in OpenAlex.
- Metabolic Engineering of Glycofusion Bispecific Antibodies for α-Dystroglycanopathies.Antibodies (Basel, Switzerland) · 2024Article
- Cell surface glycan engineering reveals that matriglycan alone can recapitulate dystroglycan binding and function.Nature communications · 2022Article
- Eyes shut homolog (EYS) interacts with matriglycan of O-mannosyl glycans whose deficiency results in EYS mislocalization and degeneration of photoreceptors.Scientific reports · 2020Article
- Recent advancements in understanding mammalian O-mannosylation.Glycobiology · 2017Review
- Article
- Article
- Differentiation-related glycan epitopes identify discrete domains of the muscle glycocalyx.Glycobiology · 2016Article
- 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
- Identification of Differentially Expressed Genes through Integrated Study of Alzheimer's Disease Affected Brain Regions.PloS one · 2016Article
- Article
- Progressive Dystrophic Pathology in Diaphragm and Impairment of Cardiac Function in FKRP P448L Mutant Mice.PloS one · 2016Article
- Matriglycan: a novel polysaccharide that links dystroglycan to the basement membrane.Glycobiology · 2015Review
- Finding the sweet spot: assembly and glycosylation of the dystrophin-associated glycoprotein complex.Anatomical record (Hoboken, N.J. : 2007) · 2014Review
- Adeno-associated virus-mediated overexpression of LARGE rescues α-dystroglycan function in dystrophic mice with mutations in the fukutin-related protein.Human gene therapy methods · 2014Article
- Mammalian O-mannosylation pathway: glycan structures, enzymes, and protein substrates.Biochemistry · 2014Review
- The transgenic expression of LARGE exacerbates the muscle phenotype of dystroglycanopathy mice.Human molecular genetics · 2014Article
- Dissecting the molecular basis of the role of the O-mannosylation pathway in disease: α-dystroglycan and forms of muscular dystrophy.Chembiochem : a European journal of chemical biology · 2013Review
- Probing the stability of the "naked" mucin-like domain of human α-dystroglycan.BMC biochemistry · 2013Article
- Biochemical and biophysical changes underlie the mechanisms of basement membrane disruptions in a mouse model of dystroglycanopathy.Matrix biology : journal of the International Society for Matrix Biology · 2013Article
- Adeno-associated viral-mediated LARGE gene therapy rescues the muscular dystrophic phenotype in mouse models of dystroglycanopathy.Human gene therapy · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Genetic defects in like-glycosyltransferase (LARGE) cause congenital muscular dystrophy with central nervous system manifestations. The underlying molecular pathomechanism is the hypoglycosylation of α-dystroglycan (α-DG), which is evidenced by diminished immunoreactivity to IIH6C4 and VIA4-1, antibodies that recognize carbohydrate epitopes. Previous studies indicate that LARGE participates in the formation of a phosphoryl glycan branch on O-linked mannose or it modifies complex N- and mucin O-glycans. In this study, we overexpressed LARGE in neural stem cells deficient in protein O-mannosyltransferase 2 (POMT2), an enzyme required for O-mannosyl glycosylation. The results showed that overexpressing LARGE did not lead to hyperglycosylation of α-DG in POMT2 knockout (KO) cells but did generate IIH6C4 and VIA4-1 immunoreactivity and laminin-binding activity. Additionally, overexpressing LARGE in cells deficient in both POMT2 and α-DG generated laminin-binding IIH6C4 immunoreactivity. These results indicate that LARGE expression resulted in the glycosylation of proteins other than α-DG in the absence of O-mannosyl glycosylation. The IIH6C4 immunoreactivity generated in double-KO cells was largely removed by treatment either with peptide N-glycosidase F or with cold aqueous hydrofluoric acid, suggesting that LARGE expression caused phosphoryl glycosylation of N-glycans. However, the glycosylation of α-DG by LARGE is dependent on POMT2, indicating that LARGE expression only modifies O-linked mannosyl glycans of α-DG. Thus, LARGE expression mediates the phosphoryl glycosylation of not only O-mannosyl glycans including those on α-DG but also N-glycans on proteins other than α-DG.
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.