Evidence map›Paper›PMID 25881155›Full record

ReviewCurrent opinion in structural biology2015

The hierarchical structural architecture of inflammasomes, supramolecular inflammatory machines.

Arthur V Hauenstein, Liman Zhang, Hao Wu

Abstract readReview
In one paragraph

Review in Current opinion in structural biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing 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

41 citing papers in PubMed.

  1. Programmable DNA Assemblies Reconstitute Supramolecular Protein Function.bioRxiv : the preprint server for biology · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Colchicine for COVID-19: targeting NLRP3 inflammasome to blunt hyperinflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  14. Review
  15. NLRP3 inflammasome activation and SARS-CoV-2-mediated hyperinflammation, cytokine storm and neurological syndromes.International journal of physiology, pathophysiology and pharmacology · 2022
    Review
  16. Article
  17. Article
  18. ATP-Binding and Hydrolysis in Inflammasome Activation.Molecules (Basel, Switzerland) · 2020
    Review
  19. The Evolutionary Origins of Programmed Cell Death Signaling.Cold Spring Harbor perspectives in biology · 2020
    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

3 authors.

Arthur V HauensteinDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, United States.
Liman ZhangDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, United States.
Hao WuDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115, United States. Electronic address: hao.wu@childrens.harvard.edu.

Funding

Structural Studies of TNF Receptor Associated Factors (TRAFs)R01AI045937 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI WU, HAO · 1999 to 2016
$5.9M
Structural & Functional Studies of TLR/IL-1R SignalingR37AI050872 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI WU, HAO · 2012 to 2021
$4.7M
Structural Studies of Protein Caspase InhibitorsR01AI050872 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI WU, HAO · 2002 to 2012
$3.6M
Molecular elucidation of the CBM complex in NF-kappaB activation by antigen recepR01AI089882 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI WU, HAO · 2010 to 2014
$1.9M
NIAID NIH HHS AI045937NIAID NIH HHS AI050872NIAID NIH HHS AI089882NIAID NIH HHS R01 AI050872
6 · The paper itself

Abstract

Inflammasomes are caspase-1 activating, molecular inflammatory machines that proteolytically mature pro-inflammatory cytokines and induce pyroptotic cell death during innate immune responses. Recent structural studies of proteins that constitute inflammasomes have yielded fresh insights into their assembly mechanisms. In particular, these include a crystal structure of the CARD-containing NOD-like receptor NLRC4, the crystallographic and electron microscopy (EM) studies of the dsDNA sensors AIM2 and IFI16, and of the regulatory protein p202, and the cryo-EM filament structure of the PYD domain of the inflammasome adapter ASC. These data suggest inflammasome assembly that starts with ligand recognition and release of autoinhibition followed by step-wise rounds of nucleated polymerization from the sensors to the adapters, then to caspase-1. In this elegant manner, inflammasomes form by an 'all-or-none' cooperative mechanism, thereby amplifying the activation of caspase-1. The dense network of filamentous structures predicted by this model has been observed in cells as micron-sized puncta.

Indexed as

AnimalsCarrier ProteinsDNA-Binding ProteinsHumansInflammasomesInflammationProtein MultimerizationCarrier ProteinsDNA-Binding ProteinsInflammasomes

Identifiers

PMID25881155
PMCPMC4476925

What OpenQuestion holds

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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.