Evidence map›Paper›PMID 42215451›Full record

ArticleNature communications2026

Non-decameric NLRP3 reveals a TGN/MTOC-distal pathway of inflammasome activation.

María Mateo-Tórtola, Inga V Hochheiser, Gaopeng Li, Lukas Funk, Atousa Hashemi, Xiao Liu, Jane Torp, Lena Erlebach, András Szolek, Jelena Grga and 6 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

16 authors.

María Mateo-TórtolaInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.ORCID 0000-0002-3412-2028
Inga V Hochheiser *Institute of Structural Biology, University of Bonn, Bonn, Germany.
Gaopeng Li *Institute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.ORCID 0000-0003-1148-7267
Lukas Funk *Institute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.ORCID 0009-0006-9441-6681
Atousa HashemiInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.ORCID 0000-0001-6352-9778
Xiao LiuInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.
Jane TorpInstitute of Structural Biology, University of Bonn, Bonn, Germany.ORCID 0000-0003-3257-8483
Lena ErlebachGerman Center for Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.ORCID 0000-0002-9077-8689
András SzolekInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.
Jelena GrgaInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.ORCID 0009-0000-3503-0160
Francesca BorkInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.ORCID 0000-0002-5073-4243
Jana S MüllerInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany.
Deborah Kronenberg-VersteegGerman Center for Neurodegenerative Diseases and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.ORCID 0000-0003-0965-9998
Matthias GeyerInstitute of Structural Biology, University of Bonn, Bonn, Germany.ORCID 0000-0002-7718-5002
Alexander N R WeberInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany. alexander.weber@uni-tuebingen.de.ORCID 0000-0002-8627-7056
Ana Tapia-AbellánInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany. ana.tapia@um.es.ORCID 0000-0002-6235-4248

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLRP3 inflammasome contributes to a wide range of conditions from infections to Alzheimer's disease. NLRP3 forms an inactive decameric cage, that upon interaction with the trans-Golgi network (TGN) and microtubule organization center (MTOC), leads to inflammasome activation, yet whether non-decamer NLRP3 species form functional inflammasomes remains unclear. Here, we design a NLRP3 exon 3 deletion variant that forms low molecular weight NLRP3 assemblies. Spatially and dynamically highly resolved microscopy in THP-1 and human macrophages shows that nigericin, a K

Indexed as

InflammasomesNLR Family, Pyrin Domain-Containing 3 Proteintrans-Golgi NetworkHumansMacrophagesMicrotubulesNeutrophilsNigericinSignal TransductionTHP-1 CellsInflammasomesNigericinNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID42215451
PMCPMC13226650

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.