ReviewCurrent molecular medicine2007
Congenital muscular dystrophies involving the O-mannose pathway.
Review in Current molecular medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 67 citations in OpenAlex.
- Emerging Roles of Dystroglycan in Cardiac Remodeling, Fibrosis, and Heart Failure.International journal of molecular sciences · 2026Review
- Expression of Dystroglycanopathy-Related Enzymes, POMGNT2 and POMGNT1, in the Mammalian Retina and 661W Cone-like Cell Line.Biomedicines · 2025Article
- Protein O-mannosylation: one sugar, several pathways, many functions.Glycobiology · 2023Review
- MS-based glycomics: An analytical tool to assess nervous system diseases.Frontiers in neuroscience · 2022Review
- A universal gene correction approach for FKRP-associated dystroglycanopathies to enable autologous cell therapy.Cell reports · 2021Article
- Decoding Neuromuscular Disorders Using Phenotypic Clusters Obtained From Co-Occurrence Networks.Frontiers in molecular biosciences · 2021Article
- Glycan Mimetics from Natural Products: New Therapeutic Opportunities for Neurodegenerative Disease.Molecules (Basel, Switzerland) · 2019Review
- Compound heterozygous POMGNT1 mutations leading to muscular dystrophy-dystroglycanopathy type A3: a case report.BMC pediatrics · 2019Article
- Overexpression of Mutant FKRP Restores Functional Glycosylation and Improves Dystrophic Phenotype in FKRP Mutant Mice.Molecular therapy. Nucleic acids · 2018Article
- Protein O-Mannosyltransferases Affect Sensory Axon Wiring and Dynamic Chirality of Body Posture in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Expression in retinal neurons of fukutin and FKRP, the protein products of two dystroglycanopathy-causative genes.Molecular vision · 2018Article
- Distinct expression of functionally glycosylated alpha-dystroglycan in muscle and non-muscle tissues of FKRP mutant mice.PloS one · 2018Article
- Efficacy of Gene Therapy Is Dependent on Disease Progression in Dystrophic Mice with Mutations in the FKRP Gene.Molecular therapy. Methods & clinical development · 2017Article
- Expression pattern in retinal photoreceptors of POMGnT1, a protein involved in muscle-eye-brain disease.Molecular vision · 2016Article
- Mammalian O-mannosylation pathway: glycan structures, enzymes, and protein substrates.Biochemistry · 2014Review
- Solving glycosylation disorders: fundamental approaches reveal complicated pathways.American journal of human genetics · 2014Review
- Adeno-associated virus 9 mediated FKRP gene therapy restores functional glycosylation of α-dystroglycan and improves muscle functions.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Identification of cell surface molecules involved in dystroglycan-independent Lassa virus cell entry.Journal of virology · 2012Article
- Glycosylated synaptomatrix regulation of trans-synaptic signaling.Developmental neurobiology · 2012Review
- Congenital protein hypoglycosylation diseases.The application of clinical genetics · 2012Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
A number of forms of congenital muscular dystrophy (CMD) have been identified that involve defects in the glycosylation of dystroglycan with O-mannosyl-linked glycans. There are at least six genes that can affect this type of glycosylation, and defects in these genes give rise to disorders that have many aspects of muscle and brain pathology in common. Overexpression of one gene implicated in CMD, LARGE, was recently shown to increase dystroglycan glycosylation and restore its function in cells taken from CMD patients. Overexpression of Galgt2, a glycosyltransferase not implicated in CMD, also alters dystroglycan glycosylation and inhibits muscular dystrophy in a mouse model of Duchenne muscular dystrophy. These findings suggest that a common approach to therapy in muscular dystrophies may be to increase the glycosylation of dystroglycan with particular glycan structures.
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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.