ArticleFrontiers in cellular neuroscience2017
Higher O-GlcNAc Levels Are Associated with Defects in Progenitor Proliferation and Premature Neuronal Differentiation during
Article in Frontiers in cellular neuroscience, 2017. 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
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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.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Genetic Rescue of Pathogenic O-GlcNAc Dyshomeostasis Associated with Microcephaly and Motor Deficits.eNeuro · 2026Article
- Zscan4 as a Candidate Conveyor of Early Developmental Defects in O-GlcNAc Transferase Intellectual Disability.Molecular & cellular proteomics : MCP · 2025Article
- O-GlcNAc transferase congenital disorder of glycosylation (OGT-CDG): Potential mechanistic targets revealed by evaluating the OGT interactome.The Journal of biological chemistry · 2024Review
- The role of O-GlcNAcylation in development.Development (Cambridge, England) · 2023Article
- O-GlcNAcylation is crucial for sympathetic neuron development, maintenance, functionality and contributes to peripheral neuropathy.Frontiers in neuroscience · 2023Article
- The O-GlcNAc cycling in neurodevelopment and associated diseases.Biochemical Society transactions · 2022Review
- Nutrient sensitive proteinLife science alliance · 2022Article
- Intellectual disability-associated disruption of O-GlcNAc cycling impairs habituation learning in Drosophila.PLoS genetics · 2022Article
- Moderate Folic Acid Supplementation in Pregnant Mice Results in Altered Sex-Specific Gene Expression in Brain of Young Mice and Embryos.Nutrients · 2022Article
- Loss of O-GlcNAcylation on MeCP2 at Threonine 203 Leads to Neurodevelopmental Disorders.Neuroscience bulletin · 2022Article
- O-GlcNAcylation in Hyperglycemic Pregnancies: Impact on Placental Function.Frontiers in endocrinology · 2021Review
- Age-related loss of neural stem cell O-GlcNAc promotes a glial fate switch through STAT3 activation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- O-GlcNAcylation regulates the methionine cycle to promote pluripotency of stem cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Klotho-Mediated Changes in Shelterin Complex Promote Cytotoxic Autophagy and Apoptosis in Amitriptyline-Treated Hippocampal Neuronal Cells.Molecular neurobiology · 2019Article
- Review
- Fine Tuning of Hepatocyte Differentiation from Human Embryonic Stem Cells: Growth FactorStem cells international · 2019Article
- Saturated fatty acid regulated lncRNA dataset duringData in brief · 2018Article
- Cross-Dysregulation ofFrontiers in endocrinology · 2018Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nutrient responsive O-GlcNAcylation is a dynamic post-translational protein modification found on several nucleocytoplasmic proteins. Previous studies have suggested that hyperglycemia induces the levels of total O-GlcNAcylation inside the cells. Hyperglycemia mediated increase in protein O-GlcNAcylation has been shown to be responsible for various pathologies including insulin resistance and Alzheimer's disease. Since maternal hyperglycemia during pregnancy is associated with adverse neurodevelopmental outcomes in the offspring, it is intriguing to identify the effect of increased protein O-GlcNAcylation on embryonic neurogenesis. Herein using human embryonic stem cells (hESCs) as model, we show that increased levels of total O-GlcNAc is associated with decreased neural progenitor proliferation and premature differentiation of cortical neurons, reduced AKT phosphorylation, increased apoptosis and defects in the expression of various regulators of embryonic corticogenesis. As defects in proliferation and differentiation during neurodevelopment are common features of various neurodevelopmental disorders, increased O-GlcNAcylation could be one mechanism responsible for defective neurodevelopmental outcomes in metabolically compromised pregnancies such as diabetes.
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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.