Evidence map›Paper›PMID 31786265›Full record

ReviewJournal of molecular biology2020

Nucleic Acid Sensors and Programmed Cell Death.

Jonathan Maelfait, Layal Liverpool, Jan Rehwinkel

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Article
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  8. Unleashing viral mimicry: A combinatorial strategy to enhance the efficacy of PARP7 inhibitors.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  9. Review
  10. Review
  11. Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024
    Review
  12. Review
  13. Trophoblast PR-SET7 dysfunction induces viral mimicry response and necroptosis associated with recurrent miscarriage.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Review
  15. Programmed Necrosis in Host Defense.Current topics in microbiology and immunology · 2023
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

3 authors at 2 institutions in 2 countries.

Jonathan MaelfaitVIB Center for Inflammation Research, 9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, 9052 Ghent, Belgium. Electronic address: jonathan.maelfait@irc.vib-ugent.be.
Layal LiverpoolMedical Research Council Human Immunology Unit, Medical Research Council Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK.
Jan RehwinkelMedical Research Council Human Immunology Unit, Medical Research Council Weatherall Institute of Molecular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford OX3 9DS, UK. Electronic address: jan.rehwinkel@imm.ox.ac.uk.
University of Oxford · GBGhent University · BE

Funding

Medical Research Council MC_UU_00008/8Wellcome Trust 100954Wellcome Trust 109024/Z/15/Z
6 · The paper itself

Abstract

Nucleic acids derived from microorganisms are powerful triggers for innate immune responses. Proteins called RNA and DNA sensors detect foreign nucleic acids and, in mammalian cells, include RIG-I, cGAS, and AIM2. On binding to nucleic acids, these proteins initiate signaling cascades that activate host defense responses. An important aspect of this defense program is the production of cytokines such as type I interferons and IL-1β. Studies conducted over recent years have revealed that nucleic acid sensors also activate programmed cell death pathways as an innate immune response to infection. Indeed, RNA and DNA sensors induce apoptosis, pyroptosis, and necroptosis. Cell death via these pathways prevents replication of pathogens by eliminating the infected cell and additionally contributes to the release of cytokines and inflammatory mediators. Interestingly, recent evidence suggests that programmed cell death triggered by nucleic acid sensors plays an important role in a number of noninfectious pathologies. In addition to nonself DNA and RNA from microorganisms, nucleic acid sensors also recognize endogenous nucleic acids, for example when cells are damaged by genotoxic agents and in certain autoinflammatory diseases. This review article summarizes current knowledge on the links between nucleic acid sensing and cell death and explores important open questions for future studies in this area.

Indexed as

Cell DeathCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDEAD Box Protein 58DNA-Binding ProteinsHumansImmunity, InnateInterferon Type IInterleukin-1betaNucleic AcidsNucleotidyltransferasesReceptors, ImmunologicRNA-Binding ProteinsAIM2 protein, humancGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDEAD Box Protein 58DNA-Binding ProteinsInterferon Type IInterleukin-1betaNucleic AcidsNucleotidyltransferasesReceptors, ImmunologicRIGI protein, humanRNA-Binding ProteinsApoptosisNecroptosisNucleic acid sensingPyroptosisType I interferon

Identifiers

PMID31786265
PMCPMC7322524
OpenAlexW2991458880

What OpenQuestion 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 OpenQuestion graph.