Evidence map›Paper›PMID 32402277›Full record

ArticleCell reports2020

Nutrient-Driven O-GlcNAcylation Controls DNA Damage Repair Signaling and Stem/Progenitor Cell Homeostasis.

Hyun-Jin Na, Ilhan Akan, Lara K Abramowitz, John A Hanover

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. PerturbingCells · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. HumanResearch square · 2025
    Article
  13. Article
  14. Preventive nutrition and food science · 2024
    Article
  15. Article
  16. CanPharmaceuticals (Basel, Switzerland) · 2024
    Review
  17. OGT and OGA: Sweet guardians of the genome.The Journal of biological chemistry · 2024
    Review
  18. The role of O-GlcNAcylation in development.Development (Cambridge, England) · 2023
    Article
  19. ProteinMetabolites · 2022
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Hyun-Jin NaLaboratory of Cellular and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Ilhan AkanLaboratory of Cellular and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Lara K AbramowitzLaboratory of Cellular and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
John A HanoverLaboratory of Cellular and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: jah@helix.nih.gov.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Targeted disruption the enzymes of O-GlcNAc cycling: Animal models of DiseaseZIADK060101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$25.7M
Intramural NIH HHS Z99 DK999999
6 · The paper itself

Abstract

Stem/progenitor cells exhibit high proliferation rates, elevated nutrient uptake, altered metabolic flux, and stress-induced genome instability. O-GlcNAcylation is an essential post-translational modification mediated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), which act in a nutrient- and stress-responsive manner. The precise role of O-GlcNAc in adult stem cells and the relationship between O-GlcNAc and the DNA damage response (DDR) is poorly understood. Here, we show that hyper-O-GlcNacylation leads to elevated insulin signaling, hyperproliferation, and DDR activation that mimic the glucose- and oxidative-stress-induced response. We discover a feedback mechanism involving key downstream effectors of DDR, ATM, ATR, and CHK1/2 that regulates OGT stability to promote O-GlcNAcylation and elevate DDR. This O-GlcNAc-dependent regulatory pathway is critical for maintaining gut homeostasis in Drosophila and the DDR in mouse embryonic stem cells (ESCs) and mouse embryonic fibroblasts (MEFs). Our findings reveal a conserved mechanistic link among O-GlcNAc cycling, stem cell self-renewal, and DDR with profound implications for stem-cell-derived diseases including cancer.

Indexed as

AnimalsDNA DamageDNA RepairHomeostasisHumansMiceN-AcetylglucosaminyltransferasesProtein Processing, Post-TranslationalSignal TransductionStem CellsN-AcetylglucosaminyltransferasesO-GlcNAc transferaseDDRDNA damage responseDrosophila intestinal stem cellISCMEFmESCmouse embryonic fibroblastmouse embryonic stem cellOGAO-GlcNAcaseO-GlcNAc transferaseO-GlcNAcylationOGT

Identifiers

PMID32402277
PMCPMC9340802
OpenAlexW3024852152

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.