ArticleGlycobiology2017
O-GlcNAc transferase regulates transcriptional activity of human Oct4.
Article in Glycobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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.
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Who cites it
32 citing papers in PubMed, 66 citations in OpenAlex.
- Pathogenic O-GlcNAc dyshomeostasis is associated with cortical malformations and hyperactivity.eLife · 2026Article
- Review
- Distinct Regions within SAP25 Recruit O-Linked Glycosylation, DNA Demethylation, and Ubiquitin Ligase and Hydrolase Activities to the Sin3/HDAC Complex.Journal of proteome research · 2024Article
- O-GlcNAcase regulates pluripotency states of human embryonic stem cells.Stem cell reports · 2024Article
- Identification of stemness-related glycosylation changes in head and neck squamous cell carcinoma.BMC cancer · 2024Article
- Neurodevelopmental defects in a mouse model of O-GlcNAc transferase intellectual disability.Disease models & mechanisms · 2024Article
- O-glycosylation of the transcription factor SPATULA promotes style development in Arabidopsis.Nature plants · 2024Article
- Diverse perspectives on proteomic posttranslational modifications to address EGFR-TKI resistance in non-small cell lung cancer.Frontiers in cell and developmental biology · 2024Review
- Review
- Article
- An O-GlcNAc transferase pathogenic variant linked to intellectual disability affects pluripotent stem cell self-renewal.Disease models & mechanisms · 2023Article
- Regulation of Primary Cilium Length by O-GlcNAc during Neuronal Development in a Human Neuron Model.Cells · 2023Article
- The role of O-GlcNAcylation in development.Development (Cambridge, England) · 2023Article
- Role of O-GlcNAcylation on cancer stem cells: Connecting nutrient sensing to cell plasticity.Advances in cancer research · 2023Review
- The O-GlcNAc cycling in neurodevelopment and associated diseases.Biochemical Society transactions · 2022Review
- Article
- Nutrients in the fate of pluripotent stem cells.Cell metabolism · 2021Review
- An Overview on the Complexity of OCT4: at the Level of DNA, RNA and Protein.Stem cell reviews and reports · 2021Review
- Biological importance of OCT transcription factors in reprogramming and development.Experimental & molecular medicine · 2021Review
- Role ofPhysiological reviews · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
O-linked β-N-acetylglucosamine (O-GlcNAc) is a single sugar modification found on many different classes of nuclear and cytoplasmic proteins. Addition of this modification, by the enzyme O-linked N-acetylglucosamine transferase (OGT), is dynamic and inducible. One major class of proteins modified by O-GlcNAc is transcription factors. O-GlcNAc regulates transcription factor properties through a variety of different mechanisms including localization, stability and transcriptional activation. Maintenance of embryonic stem (ES) cell pluripotency requires tight regulation of several key transcription factors, many of which are modified by O-GlcNAc. Octamer-binding protein 4 (Oct4) is one of the key transcription factors required for pluripotency of ES cells and more recently, the generation of induced pluripotent stem (iPS) cells. The action of Oct4 is modulated by the addition of several post-translational modifications, including O-GlcNAc. Previous studies in mice found a single site of O-GlcNAc addition responsible for transcriptional regulation. This study was designed to determine if this mechanism is conserved in humans. We mapped 10 novel sites of O-GlcNAc attachment on human Oct4, and confirmed a role for OGT in transcriptional activation of Oct4 at a site distinct from that found in mouse that allows distinction between different Oct4 target promoters. Additionally, we uncovered a potential new role for OGT that does not include its catalytic function. These results confirm that human Oct4 activity is being regulated by OGT by a mechanism that is distinct from mouse Oct4.
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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.