Evidence map›Paper›PMID 30518920›Full record

ArticleNature communications2018

NLRP3 lacking the leucine-rich repeat domain can be fully activated via the canonical inflammasome pathway.

Iva Hafner-Bratkovič, Petra Sušjan, Duško Lainšček, Ana Tapia-Abellán, Kosta Cerović, Lucija Kadunc, Diego Angosto-Bazarra, Pablo Pelegrin, Roman Jerala

Abstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing 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

85 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. AI platform for CRISPR functional mapping and function-based drug design.bioRxiv : the preprint server for biology · 2026
    Article
  6. Review
  7. Diverse Scaffolds Facilitate NLRP3 Clustering and Inflammasome Formation in Response to Perturbations in Cell Homeostasis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Journal of inflammation research · 2025
    Review
  19. Review
  20. Review

25 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

9 authors.

Iva Hafner-BratkovičDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Hajdrihova 19, 1000, Ljubljana, Slovenia. iva.hafner@ki.si.ORCID http://orcid.org/0000-0001-5635-931X
Petra SušjanDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Hajdrihova 19, 1000, Ljubljana, Slovenia.ORCID http://orcid.org/0000-0002-0133-9896
Duško LainščekDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Hajdrihova 19, 1000, Ljubljana, Slovenia.
Ana Tapia-AbellánMolecular Inflammation Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, Carretera Buenavista s/n, 30120 El Palmar, Murcia, Spain.
Kosta CerovićDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Hajdrihova 19, 1000, Ljubljana, Slovenia.ORCID http://orcid.org/0000-0001-9585-0347
Lucija KaduncDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Hajdrihova 19, 1000, Ljubljana, Slovenia.
Diego Angosto-BazarraMolecular Inflammation Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, Carretera Buenavista s/n, 30120 El Palmar, Murcia, Spain.
Pablo PelegrinMolecular Inflammation Group, Biomedical Research Institute of Murcia (IMIB-Arrixaca), University Clinical Hospital Virgen de la Arrixaca, Carretera Buenavista s/n, 30120 El Palmar, Murcia, Spain.ORCID http://orcid.org/0000-0002-9688-1804
Roman JeralaDepartment of Synthetic Biology and Immunology, National Institute of Chemistry, Hajdrihova 19, 1000, Ljubljana, Slovenia. roman.jerala@ki.si.ORCID http://orcid.org/0000-0002-6337-5251

Funding

European Research Council 614578
6 · The paper itself

Abstract

NLRP3 is a cytosolic sensor triggered by different pathogen- and self-derived signals that plays a central role in a variety of pathological conditions, including sterile inflammation. The leucine-rich repeat domain is present in several innate immune receptors, where it is frequently responsible for sensing danger signals and regulation of activation. Here we show by reconstitution of truncated and chimeric variants into Nlrp3

Indexed as

AnimalsApoptosis Regulatory ProteinsCalcium-Binding ProteinsFemaleHumansInflammasomesInflammationLeucineMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinProtein DomainsApoptosis Regulatory ProteinsCalcium-Binding ProteinsInflammasomesIpaf protein, mouseLeucineNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouse

Identifiers

PMID30518920
PMCPMC6281599

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.