Evidence map›Paper›PMID 29196474›Full record

ReviewJournal of cell science2017

Inflammasome activation and assembly at a glance.

Ankit Malik, Thirumala-Devi Kanneganti

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers.

0numbers the graph read from it
0cells of the map it votes in
266citing papers in PubMed
13.1field-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

266 citing papers in PubMed, 441 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. A century of cell death research.Journal of cell science · 2026
    Review
  6. Article
  7. Tubuloside B Alleviates AβNeurotoxicity research · 2026
    Article
  8. Article
  9. Review
  10. Research progress in PANoptosis mechanisms and their interplay with tuberculosis.Frontiers in cellular and infection microbiology · 2026
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. PANoptosis: a potential target of atherosclerotic cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2025
    Review
  17. Mitigation of nicotine-induced podocyte injury through inhibition of thioredoxin interacting protein.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Article
  18. Review
  19. Review
  20. Article

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

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

2 authors at 1 institution in 1 country.

Ankit MalikDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA thirumala-devi.kanneganti@stjude.org.ORCID http://orcid.org/0000-0002-6395-6443
St. Jude Children's Research Hospital · US

Funding

Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
The Non-Inflammasome NLRs in Immunity and Host defenseR01AI124346 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2016 to 2026
$5.8M
Inflammatory Caspases in Innate Immunity and InflammationR37AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2017 to 2026
$4.9M
NLR signaling in colitis and colorectal tumorigenesisR01CA163507 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2020
$3.5M
Inflammatory Caspases in Innate Immunity and InflammationR01AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2016
$2.2M
NCI NIH HHS R01 CA163507NIAID NIH HHS R01 AI101935NIAID NIH HHS R01 AI124346NIAID NIH HHS R37 AI101935NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

Inflammasomes are multimeric protein complexes that typically comprise a sensor, an adaptor and the zymogen procaspase-1. An inflammasome assembles in response to a diverse range of pathogen-associated or danger-associated molecular patterns (PAMPs or DAMPs). The inflammasome platform leads to activation of caspase-1 through proximity-induced self-cleavage, which further induces maturation of interleukins 1β and 18 (IL-1β and IL-18) through proteolytic cleavage of pro-IL-1β and pro-IL-18. Activated caspase-1 also cleaves gasdermin D, which leads to a particular form of cell death called pyroptosis. Mutations in genes that encode inflammasome components are associated with many inflammatory disorders, and studies in the past decade have highlighted the importance of appropriate activation of the inflammasome in homeostasis and disease pathogenesis. Therefore, much attention is being paid to uncover the modulators and regulators of inflammasome assembly and pyroptosis. This Cell Science at a Glance article and accompanying poster outlines the concepts in the activation of inflammasome sensors and assembly of the inflammasome platform. We also discuss recent insights into the mechanisms of regulation of inflammasome activity and the induction of cell death by pyroptosis.

Indexed as

AnimalsCell DeathHumansInflammasomesInterleukin-18Interleukin-1betaProtein MultimerizationPyroptosisInflammasomesInterleukin-18Interleukin-1betaCell deathIL-1 cytokinesInflammasomePyroptosis

Identifiers

PMID29196474
PMCPMC5769591
OpenAlexW2775627464

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.