Evidence map›Paper›PMID 27374331›Full record

ArticleCell2016

Hexokinase Is an Innate Immune Receptor for the Detection of Bacterial Peptidoglycan.

Andrea J Wolf, Christopher N Reyes, Wenbin Liang, Courtney Becker, Kenichi Shimada, Matthew L Wheeler, Hee Cheol Cho, Narcis I Popescu, K Mark Coggeshall, Moshe Arditi and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 341 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
341citing papers in PubMed, 1 pooled it
25.6field-weighted citation impact, top 1% 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

341 citing papers in PubMed, 1 synthesis or guideline pooled it, 547 citations in OpenAlex.

  1. Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023
    Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Infection and immunity · 2026
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026
    Review

281 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Andrea J WolfF. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Christopher N ReyesF. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Wenbin LiangCedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Courtney BeckerF. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Kenichi ShimadaDivision of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Matthew L WheelerF. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Hee Cheol ChoCedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Narcis I PopescuImmunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
K Mark CoggeshallImmunobiology and Cancer Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
Moshe ArditiDivision of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Pediatric Infectious Diseases, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
David M UnderhillF. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Division of Immunology, Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. Electronic address: david.underhill@csmc.edu.
Cedars-Sinai Medical Center · USOklahoma Medical Research Foundation · US

Funding

Translation of immunologic technologies from basic research into pre-clinical nonU19AI062629 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 2004 to 2023
$56.2M
Phagosomal targeting of CARD proteinsR01GM085796 · NIGMS · CEDARS-SINAI MEDICAL CENTER · PI UNDERHILL, DAVID M. · 2008 to 2020
$4.1M
Molecular determinants of the cardiac pacemaker automaticityR01HL111646 · NHLBI · EMORY UNIVERSITY · PI CHO, HEE CHEOL · 2012 to 2016
$2.0M
Role of Innate Immunity in Pathogenesis of Chlamydia Pneumonia InfectionR01AI067995 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2006 to 2010
$1.9M
The Cedars-Sinai Immunobiology Training ProgramT32AI089553 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE, TARGAN, STEPHAN R. · 2010 to 2016
$1.1M
Innate Immunity and Host Responses in Pathogenesis of Chlamydia PneumoniaeR56AI067995 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2012 to 2012
$413k
NHLBI NIH HHS R01 HL111646NIAID NIH HHS R01 AI067995NIAID NIH HHS R56 AI067995NIAID NIH HHS T32 AI089553NIAID NIH HHS U19 AI062629NIGMS NIH HHS R01 GM085796
6 · The paper itself

Abstract

Degradation of Gram-positive bacterial cell wall peptidoglycan in macrophage and dendritic cell phagosomes leads to activation of the NLRP3 inflammasome, a cytosolic complex that regulates processing and secretion of interleukin (IL)-1β and IL-18. While many inflammatory responses to peptidoglycan are mediated by detection of its muramyl dipeptide component in the cytosol by NOD2, we report here that NLRP3 inflammasome activation is caused by release of N-acetylglucosamine that is detected in the cytosol by the glycolytic enzyme hexokinase. Inhibition of hexokinase by N-acetylglucosamine causes its dissociation from mitochondria outer membranes, and we found that this is sufficient to activate the NLRP3 inflammasome. In addition, we observed that glycolytic inhibitors and metabolic conditions affecting hexokinase function and localization induce inflammasome activation. While previous studies have demonstrated that signaling by pattern recognition receptors can regulate metabolic processes, this study shows that a metabolic enzyme can act as a pattern recognition receptor. PAPERCLIP.

Indexed as

AcetylationAcetylglucosamineAnimalsBacillus anthracisCell WallDendritic CellsGlycolysisHexokinaseHumansInflammasomesMiceMice, Inbred C57BLMitochondriaModels, BiologicalMonocytesNLR Family, Pyrin Domain-Containing 3 ProteinAcetylglucosamineHexokinaseInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePeptidoglycanPotassiumReceptors, Immunologic

Identifiers

PMID27374331
PMCPMC5534359
OpenAlexW2460289322

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.