Evidence map›Paper›PMID 28409545›Full record

ArticleInnate immunity2017

High-affinity caspase-4 binding to LPS presented as high molecular mass aggregates or in outer membrane vesicles.

Mark A Wacker, Athmane Teghanemt, Jerrold P Weiss, Jason H Barker

Open access · bronzeAbstract read
In one paragraph

Article in Innate immunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. ALDH2 Mediated Ferroptosis Regulation in Ischemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2026
    Review
  3. Review
  4. Recognition ofJournal of oral microbiology · 2025
    Article
  5. Article
  6. LPS-aggregating proteins GBP1 and GBP2 are each sufficient to enhance caspase-4 activation both in cellulo and in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Review
  8. Article
  9. Review
  10. An overview of the non-canonical inflammasome.Molecular aspects of medicine · 2020
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Innate immunity to intracellular LPS.Nature immunology · 2019
    Review
  18. 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 at 2 institutions in 1 country.

Mark A Wacker1 Department of Biology, Central Michigan University, Mt. Pleasant, MI, USA.
Athmane Teghanemt2 Inflammation Program, University of Iowa, and Iowa City VA Health Care System, Iowa City, IA, USA.
Jerrold P Weiss2 Inflammation Program, University of Iowa, and Iowa City VA Health Care System, Iowa City, IA, USA.
Jason H Barker2 Inflammation Program, University of Iowa, and Iowa City VA Health Care System, Iowa City, IA, USA.
University of Iowa · USCentral Michigan University · US

Funding

Pulmonary Toxicology Facility CoreP30ES005605 · NIEHS · UNIVERSITY OF IOWA · PI Brandi Janssen · 1990 to 2026
$40.5M
Studies of the capsular-like antigen of F. tularensisP01AI044642 · NIAID · UNIVERSITY OF IOWA · PI APICELLA, MICHAEL A. · 1999 to 2014
$18.2M
The Structural Determinants of Innate Immune Modulation by Francisella LPSR01AI104728 · NIAID · UNIVERSITY OF IOWA · PI BARKER, JASON HOLT · 2014 to 2018
$1.9M
NIAID NIH HHS P01 AI044642NIAID NIH HHS R01 AI104728NIEHS NIH HHS P30 ES005605
6 · The paper itself

Abstract

Caspases of the non-canonical inflammasome (caspases -4, -5, and -11) directly bind endotoxin (LOS/LPS) and can be activated in the absence of any co-factors. Models of LPS-induced caspase activation have postulated that 1:1 binding of endotoxin monomers to caspase trigger caspase oligomerization and activation, analogous to that established for endotoxin-induced activation of MD-2/TLR4. However, using metabolically radiolabeled LOS and LPS, we now show high affinity and selective binding of caspase-4 to high molecular mass aggregates of purified endotoxin and to endotoxin-rich outer membrane vesicles without formation of 1:1 endotoxin:caspase complexes. Thus, our findings demonstrate markedly different endotoxin recognition properties of caspase-4 from that of MD-2/TLR4 and strongly suggest that activation of caspase-4 (and presumably caspase-5 and caspase-11) are mediated by interactions with activating endotoxin-rich membrane interfaces rather than by endotoxin monomers.

Indexed as

Caspases, InitiatorCell WallCytoplasmic VesiclesHumansLipopolysaccharidesMitochondrial MembranesNeisseria meningitidisProtein BindingProtein MultimerizationProtoplastsRecombinant ProteinsStaphylococcus aureusCASP4 protein, humanCaspases, InitiatorLipopolysaccharidesRecombinant Proteinscaspase-11Caspase-4lipopolysaccharidenon-canonical inflammasomeouter membrane vesicle

Identifiers

PMID28409545
PMCPMC5540323
OpenAlexW2592650543

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.