Evidence map›Paper›PMID 28576828›Full record

ArticleThe Journal of biological chemistry2017

The intracellular chloride channel proteins CLIC1 and CLIC4 induce IL-1β transcription and activate the NLRP3 inflammasome.

Raquel Domingo-Fernández, Rebecca C Coll, Jay Kearney, Samuel Breit, Luke A J O'Neill

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

100 citing papers in PubMed, 160 citations in OpenAlex.

  1. Trial
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  8. Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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  15. Anti-Inflammatory and Survival Benefits of Dipeptidyl Peptidase 4 Inhibitors Among Patients with Gout, T2DM Patients and Chronic Kidney Disease.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2025
    Article
  16. Review
  17. Intracellular Chloride Channels: A Rising Target in Lung Disease Research.Journal of respiratory biology and translational medicine · 2025
    Article
  18. Article
  19. Review
  20. Review

40 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

5 authors at 3 institutions in 2 countries.

Raquel Domingo-FernándezSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Pearse Street, Dublin 2, Ireland.
Rebecca C CollInstitute for Molecular Bioscience (IMB), IMB Centre for Inflammation and Disease Research, The University of Queensland, Brisbane, St Lucia, Queensland 4072, Australia.
Jay KearneySchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Pearse Street, Dublin 2, Ireland.
Samuel BreitSt. Vincent's Centre for Applied Medical Research, St. Vincent's Hospital and University of New South Wales, Sydney, New South Wales 2010, Australia.
Luke A J O'NeillSchool of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Pearse Street, Dublin 2, Ireland. Electronic address: laoneill@tcd.ie.
Trinity College Dublin · IESt Vincent's Hospital Sydney · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLRP3 inflammasome is a multiprotein complex that regulates the activation of caspase-1 leading to the maturation of the proinflammatory cytokines IL-1β and IL-18 and promoting pyroptosis. Classically, the NLRP3 inflammasome in murine macrophages is activated by the recognition of pathogen-associated molecular patterns and by many structurally unrelated factors. Understanding the precise mechanism of NLRP3 activation by such a wide array of stimuli remains elusive, but several signaling events, including cytosolic efflux and influx of select ions, have been suggested. Accordingly, several studies have indicated a role of anion channels in NLRP3 inflammasome assembly, but their direct involvement has not been shown. Here, we report that the chloride intracellular channel proteins CLIC1 and CLIC4 participate in the regulation of the NLRP3 inflammasome. Confocal microscopy and cell fractionation experiments revealed that upon LPS stimulation of macrophages, CLIC1 and CLIC4 translocated into the nucleus and cellular membrane. In LPS/ATP-stimulated bone marrow-derived macrophages (BMDMs), CLIC1 or CLIC4 siRNA transfection impaired transcription of IL-1β, ASC speck formation, and secretion of mature IL-1β. Collectively, our results demonstrate that CLIC1 and CLIC4 participate both in the priming signal for IL-1β and in NLRP3 activation.

Indexed as

Active Transport, Cell NucleusAnimalsBone Marrow CellsCell LineCells, CulturedChloride ChannelsInflammasomesInterleukin-1betaLipopolysaccharidesMacrophage ActivationMacrophagesMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMitochondrial ProteinsChloride ChannelsClic1 protein, mouseCLIC protein, mouseIL1B protein, mouseInflammasomesInterleukin-1betaLipopolysaccharidesMitochondrial ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousechloride channelCLIC1CLIC4IL-1βinflammasomelipopolysaccharide (LPS)macrophageNLRP3

Identifiers

PMID28576828
PMCPMC5519359
OpenAlexW2621370764

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.