ArticleCell reports2017
A Conserved Splicing Silencer Dynamically Regulates O-GlcNAc Transferase Intron Retention and O-GlcNAc Homeostasis.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 127 citations in OpenAlex.
- Tools for investigating O-GlcNAc in signaling and other fundamental biological pathways.The Journal of biological chemistry · 2024Pooled it
- The human O-GlcNAcome database and meta-analysis.Scientific data · 2021Pooled it
- Chemical biology tools for the O-GlcNAc modification: Determining systems-level functions and druggability.Current opinion in chemical biology · 2026Review
- iMPI: An Integrative Database for MicroProteins Encoded by Intron Retention in Tumors.Proteomics · 2026Article
- Review
- Genetic manipulation of OGT enhances NK cell-mediated cytotoxicity in tumor immunity.Journal of advanced research · 2026Article
- Hcfc1 and Ogt Mediate Zebrafish CNS Regeneration Through Hippo/Yap Signalling.Cell proliferation · 2026Article
- Small molecule splicing modulators that disrupt O-GlcNAc homeostasis.Nature communications · 2026Article
- Dissecting the Mechanisms Underlying Substrate Recognition and Functional Regulation of O-GlcNAc Cycling Enzymes.ACS chemical biology · 2025Review
- A Genetically Encoded Assay System to Quantify O-GlcNAc Transferase (OGT) Activity in Live Cells.Angewandte Chemie (International ed. in English) · 2025Article
- An alternative cytoplasmic SFPQ isoform with reduced phase separation potential is up-regulated in ALS.Science advances · 2025Article
- O-GlcNAc modulation of nuclear pore complexes orchestrates mRNA export efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Nuclear pore complex protein RANBP2 and related SUMOylation in solid malignancies.Genes & diseases · 2025Review
- Linking O-GlcNAc and intron retention.eLife · 2025Article
- Article
- O-GlcNAcylation in Endocrinology: The Sweet Link.Endocrinology · 2025Review
- Perturbing nuclear glycosylation in the mouse preimplantation embryo slows down embryonic development.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Exploiting O-GlcNAc dyshomeostasis to screen O-GlcNAc transferase intellectual disability variants.Stem cell reports · 2025Article
- Genetic gradual reduction of OGT activity unveils the essential role of O-GlcNAc in the mouse embryo.PLoS genetics · 2025Article
- Compromised CDK12 activity causes dependency on the high activity of O-GlcNAc transferase.Glycobiology · 2024Article
14 more citing papers are in PubMed but not listed here.
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
Abstract
Modification of nucleocytoplasmic proteins with O-GlcNAc regulates a wide variety of cellular processes and has been linked to human diseases. The enzymes O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) add and remove O-GlcNAc, but the mechanisms regulating their expression remain unclear. Here, we demonstrate that retention of the fourth intron of OGT is regulated in response to O-GlcNAc levels. We further define a conserved intronic splicing silencer (ISS) that is necessary for OGT intron retention. Deletion of the ISS in colon cancer cells leads to increases in OGT, but O-GlcNAc homeostasis is maintained by concomitant increases in OGA protein. However, the ISS-deleted cells are hypersensitive to OGA inhibition in culture and in soft agar. Moreover, growth of xenograft tumors from ISS-deleted cells is compromised in mice treated with an OGA inhibitor. Thus, ISS-mediated regulation of OGT intron retention is a key component in OGT expression and maintaining O-GlcNAc homeostasis.
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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.