Evidence map›Paper›PMID 29191979›Full record

ArticleEMBO reports2018

Shigella hijacks the glomulin-cIAPs-inflammasome axis to promote inflammation.

Shiho Suzuki, Toshihiko Suzuki, Hitomi Mimuro, Tsunehiro Mizushima, Chihiro Sasakawa

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 26 citations in OpenAlex.

  1. ThebioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Pyroptosis in microbial infectious diseases.Molecular biology reports · 2023
    Review
  6. The NEL Family of Bacterial E3 Ubiquitin Ligases.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. NLRP3 inflammasome activation and cell death.Cellular & molecular immunology · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Use of zebrafish to studyDisease models & mechanisms · 2018
    Review
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

5 authors at 4 institutions in 1 country.

Shiho SuzukiDivision of Bacterial Infection Biology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan ss.bact@tmd.ac.jp sasakawa@ims.u-tokyo.ac.jp.ORCID 0000-0003-3168-1729
Toshihiko SuzukiDepartment of Bacterial Infection and Host Response, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Hitomi MimuroDivision of Bacteriology, Department of Infectious Diseases Control, International Research Center for Infectious Diseases, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Tsunehiro MizushimaPicobiology Institute, Graduate School of Life Science, University of Hyogo, Hyogo, Japan.
Chihiro SasakawaDivision of Bacterial Infection Biology, Institute of Medical Science, The University of Tokyo, Tokyo, Japan ss.bact@tmd.ac.jp sasakawa@ims.u-tokyo.ac.jp.ORCID 0000-0002-6919-1832
Tokyo Medical and Dental University · JPChiba University Hospital · JPNational Institute of Infectious Diseases · JPUniversity of Hyogo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Shigella deploys a unique mechanism to manipulate macrophage pyroptosis by delivering the IpaH7.8 E3 ubiquitin ligase via its type III secretion system. IpaH7.8 ubiquitinates glomulin (GLMN) and elicits its degradation, thereby inducing inflammasome activation and pyroptotic cell death of macrophages. Here, we show that GLMN specifically binds cellular inhibitor of apoptosis proteins 1 and 2 (cIAP1 and cIAP2), members of the inhibitor of apoptosis (IAP) family of RING-E3 ligases, which results in reduced E3 ligase activity, and consequently inflammasome-mediated death of macrophages. Importantly, reducing the levels of GLMN in macrophages via IpaH7.8, or siRNA-mediated knockdown, enhances inflammasome activation in response to infection by Shigella, Salmonella, or Pseudomonas, stimulation with NLRP3 inflammasome activators (including SiO

Indexed as

Host-Pathogen InteractionsAmino Acid SequenceAnimalsAntigens, BacterialBacterial ProteinsCarrier ProteinsGene Expression RegulationInflammasomesInhibitor of Apoptosis ProteinsIsoenzymesMacrophagesMiceMice, Inbred C57BLMuscle ProteinsPrimary Cell CultureProtein BindingAntigens, BacterialBacterial ProteinsBirc4 protein, mouseCarrier Proteinsglomulin protein, mouseInflammasomesInhibitor of Apoptosis ProteinsipaH protein, Shigella flexneriIsoenzymesMuscle ProteinsRBX1 protein, mouseType III Secretion SystemscIAPsGLMNinflammasome activationShigella

Identifiers

PMID29191979
PMCPMC5757219
OpenAlexW2772264713

What OpenQuestion holds

Textmetadata
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.