ArticleThe Journal of biological chemistry
Loss of O-GlcNAcase catalytic activity leads to defects in mouse embryogenesis.
Article in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- Genetic Rescue of Pathogenic O-GlcNAc Dyshomeostasis Associated with Microcephaly and Motor Deficits.eNeuro · 2026Article
- The Glyco-Switch of life: O-GlcNAcylation in cell fate decision.Glycobiology · 2025Review
- Zscan4 as a Candidate Conveyor of Early Developmental Defects in O-GlcNAc Transferase Intellectual Disability.Molecular & cellular proteomics : MCP · 2025Article
- Protein O-GlcNAcylation in reproductive biology and the impact of metabolic disease.Human reproduction update · 2025Review
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- Review
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- Article
- Neurodevelopmental defects in a mouse model of O-GlcNAc transferase intellectual disability.Disease models & mechanisms · 2024Article
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- Understanding and exploiting the roles of O-GlcNAc in neurodegenerative diseases.The Journal of biological chemistry · 2023Review
- An O-GlcNAc transferase pathogenic variant linked to intellectual disability affects pluripotent stem cell self-renewal.Disease models & mechanisms · 2023Article
- The role of O-GlcNAcylation in development.Development (Cambridge, England) · 2023Article
- Emerging Role of Protein O-GlcNAcylation in Liver Metabolism: Implications for Diabetes and NAFLD.International journal of molecular sciences · 2023Review
- The O-GlcNAc cycling in neurodevelopment and associated diseases.Biochemical Society transactions · 2022Review
- Review
- Review
- O-GlcNAcylation in Renal (Patho)Physiology.International journal of molecular sciences · 2022Review
- ProteinMetabolites · 2022Review
- Protein O-GlcNAcylation and the regulation of energy homeostasis: lessons from knock-out mouse models.Journal of biomedical science · 2022Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
O-GlcNAcylation is an essential post-translational modification that has been implicated in neurodevelopmental and neurodegenerative disorders. O-GlcNAcase (OGA), the sole enzyme catalyzing the removal of O-GlcNAc from proteins, has emerged as a potential drug target. OGA consists of an N-terminal OGA catalytic domain and a C-terminal pseudo histone acetyltransferase (HAT) domain with unknown function. To investigate phenotypes specific to loss of OGA catalytic activity and dissect the role of the HAT domain, we generated a constitutive knock-in mouse line, carrying a mutation of a catalytic aspartic acid to alanine. These mice showed perinatal lethality and abnormal embryonic growth with skewed Mendelian ratios after day E18.5. We observed tissue-specific changes in O-GlcNAc homeostasis regulation to compensate for loss of OGA activity. Using X-ray microcomputed tomography on late gestation embryos, we identified defects in the kidney, brain, liver, and stomach. Taken together, our data suggest that developmental defects during gestation may arise upon prolonged OGA inhibition specifically because of loss of OGA catalytic activity and independent of the function of the HAT domain.
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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.