Evidence map›Paper›PMID 39289506›Full record

ArticleCell death and differentiation2024

Retention of ES cell-derived 129S genome drives NLRP1 hypersensitivity and transcriptional deregulation in Nlrp3

Felix D Weiss, Yubell Alvarez, Farhad Shakeri, Anshupa Sahu, Petro Leka, Alesja Dernst, Jessika Rollheiser, Matilde Vasconcelos, Adriana Geraci, Fraser Duthie and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Felix D WeissInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany. fweiss@uni-bonn.de.ORCID 0000-0003-0228-5081
Yubell AlvarezInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany.
Farhad ShakeriInstitute for Medical Biometry, Informatics and Epidemiology, Medical Faculty, University Hospital Bonn, Bonn, Germany.
Anshupa SahuInstitute for Medical Biometry, Informatics and Epidemiology, Medical Faculty, University Hospital Bonn, Bonn, Germany.
Petro LekaInstitute of Innate Immunity, Department for Innate Immunity & Metaflammation, Medical Faculty, University of Bonn, Bonn, Germany.
Alesja DernstInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany.
Jessika RollheiserInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany.
Matilde VasconcelosInstitute of Innate Immunity, Department for Innate Immunity & Metaflammation, Medical Faculty, University of Bonn, Bonn, Germany.
Adriana GeraciInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany.
Fraser DuthieInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany.
Rainer StahlInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany.
Hye Eun LeeInstitute of Innate Immunity, Department for Innate Immunity & Metaflammation, Medical Faculty, University of Bonn, Bonn, Germany.
Anne-Kathrin GellnerDepartment of Psychiatry and Psychotherapy, University Hospital Bonn, Bonn, Germany.
Andreas BunessInstitute for Medical Biometry, Informatics and Epidemiology, Medical Faculty, University Hospital Bonn, Bonn, Germany.
Eicke LatzInstitute of Innate Immunity, Department for Innate Immunity & Metaflammation, Medical Faculty, University of Bonn, Bonn, Germany.
Felix MeissnerInstitute of Innate Immunity, Department for Systems Immunology and Proteomics, Medical Faculty, University of Bonn, Bonn, Germany. felix.meissner@uni-bonn.de.ORCID 0000-0003-1000-7989

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) EXC2151 - 390873048Deutsche Forschungsgemeinschaft (German Research Foundation) GRK2168 - 272482170Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1402 - 414786233Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1454 - 432325352Deutsche Forschungsgemeinschaft (German Research Foundation) TRR237 - 369799452EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) No. 848146 (To_Aition)Helmholtz Association ZT-0027
6 · The paper itself

Abstract

Immune response genes are highly polymorphic in humans and mice, with heterogeneity amongst loci driving strain-specific host defence responses. The inadvertent retention of polymorphic loci can introduce confounding phenotypes, leading to erroneous conclusions, and impeding scientific advancement. In this study, we employ a combination of RNAseq and variant calling analyses to identify a substantial region of 129S genome, including the highly polymorphic Nlrp1 locus, proximal to Nlrp3, in one of the most commonly used mouse models of NLRP3 deficiency (Nlrp3

Indexed as

Adaptor Proteins, Signal TransducingNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsApoptosis Regulatory ProteinsGenomeInflammasomesMacrophagesMiceMice, Inbred C57BLAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsInflammasomesNALP1 protein, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouse

Identifiers

PMID39289506
PMCPMC11618613

What OpenQuestion holds

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Registered trials

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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.