Evidence map›Paper›PMID 25474640›Full record

ArticlePloS one2014

Conserved nutrient sensor O-GlcNAc transferase is integral to C. elegans pathogen-specific immunity.

Michelle R Bond, Salil K Ghosh, Peng Wang, John A Hanover

Abstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
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

20 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Role of UDP-Glycosyltransferase (Chemical research in toxicology · 2024
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Neuro-immune communication inCurrent research in immunology · 2021
    Article
  10. Article
  11. Molecular Interrogation to Crack the Case of O-GlcNAc.Chemistry (Weinheim an der Bergstrasse, Germany) · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. The Inducible Response of the NematodeFrontiers in microbiology · 2019
    Article
  17. Review
  18. RSC advances · 2018
    Article
  19. Article
  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.

Michelle R BondNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Salil K GhoshCenter for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland, United States of America.
Peng WangDepartment of Pathology, Medstar Georgetown University Hospital, Washington, District of Columbia, United States of America.
John A HanoverNational Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.

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
Enzymes of O-GlcNAc cycling linked to type-2 diabetes and neurodegenerationZIADK060103 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$20.8M
Calmodulin-driven Nuclear Trafficking linked to diabetes and insulin signalingZIADK060102 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$8.5M
Intramural NIH HHS
6 · The paper itself

Abstract

Discriminating pathogenic bacteria from bacteria used as a food source is key to Caenorhabidits elegans immunity. Using mutants defective in the enzymes of O-linked N-acetylglucosamine (O-GlcNAc) cycling, we examined the role of this nutrient-sensing pathway in the C. elegans innate immune response. Genetic analysis showed that deletion of O-GlcNAc transferase (ogt-1) yielded animals hypersensitive to the human pathogen S. aureus but not to P. aeruginosa. Genetic interaction studies revealed that nutrient-responsive OGT-1 acts through the conserved β-catenin (BAR-1) pathway and in concert with p38 MAPK (PMK-1) to modulate the immune response to S. aureus. Moreover, whole genome transcriptional profiling revealed that O-GlcNAc cycling mutants exhibited deregulation of unique stress- and immune-responsive genes. The participation of nutrient sensor OGT-1 in an immunity module evolutionarily conserved from C. elegans to humans reveals an unexplored nexus between nutrient availability and a pathogen-specific immune response.

Indexed as

AcetylglucosamineAnimalsbeta CateninCaenorhabditis elegansFoodHumansImmunity, InnateN-Acetylglucosaminyltransferasesp38 Mitogen-Activated Protein KinasesSignal TransductionStaphylococcus aureusAcetylglucosaminebeta CateninN-AcetylglucosaminyltransferasesO-GlcNAc transferasep38 Mitogen-Activated Protein Kinases

Identifiers

PMID25474640
PMCPMC4256294

What OpenQuestion holds

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Registered trials

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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.