Evidence map›Paper›PMID 36869180›Full record

ArticleCell death and differentiation2023

A noncanonical response to replication stress protects genome stability through ROS production, in an adaptive manner.

Sandrine Ragu, Nathalie Droin, Gabriel Matos-Rodrigues, Aurélia Barascu, Sylvain Caillat, Gabriella Zarkovic, Capucine Siberchicot, Elodie Dardillac, Camille Gelot, Josée Guirouilh-Barbat and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

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  11. Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023
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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

15 authors at 4 institutions in 1 country.

Sandrine RaguUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, 24 rue du Faubourg St. Jacques, 75014, Paris, France.
Nathalie DroinInstitut de Cancérologie Gustave-Roussy, INSERM U1287, Université Paris Saclay, Equipe Labellisée Ligue Contre le Cancer 114 Rue Edouard Vaillant, 94805, Villejuif, France.
Gabriel Matos-RodriguesUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, 24 rue du Faubourg St. Jacques, 75014, Paris, France.
Aurélia BarascuUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, 24 rue du Faubourg St. Jacques, 75014, Paris, France.
Sylvain CaillatIRIG/DIESE/SyMMES/CIBEST, UMR 5819 CEA/CNRS/UGA, CEA Grenoble, 38054, Grenoble, France.
Gabriella ZarkovicGroup "Mechanisms of DNA Repair and Carcinogenesis", Gustave Roussy Cancer Campus, CNRS UMR9019, Université Paris-Saclay, 94805, Villejuif, France.
Capucine SiberchicotUniversité Paris-Saclay, Université Paris-Cité, CEA/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, F-92260, Fontenay-aux-Roses, France.
Elodie DardillacUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, 24 rue du Faubourg St. Jacques, 75014, Paris, France.ORCID 0000-0002-2069-8309
Camille GelotUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, 24 rue du Faubourg St. Jacques, 75014, Paris, France.
Josée Guirouilh-BarbatUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, 24 rue du Faubourg St. Jacques, 75014, Paris, France.
J Pablo RadicellaUniversité Paris-Saclay, Université Paris-Cité, CEA/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, F-92260, Fontenay-aux-Roses, France.
Alexander A IshchenkoGroup "Mechanisms of DNA Repair and Carcinogenesis", Gustave Roussy Cancer Campus, CNRS UMR9019, Université Paris-Saclay, 94805, Villejuif, France.
Jean-Luc RavanatIRIG/DIESE/SyMMES/CIBEST, UMR 5819 CEA/CNRS/UGA, CEA Grenoble, 38054, Grenoble, France.
Eric SolaryInstitut de Cancérologie Gustave-Roussy, INSERM U1287, Université Paris Saclay, Equipe Labellisée Ligue Contre le Cancer 114 Rue Edouard Vaillant, 94805, Villejuif, France.
Bernard S LopezUniversité de Paris, INSERM U1016, UMR 8104 CNRS, Institut Cochin, 24 rue du Faubourg St. Jacques, 75014, Paris, France. bernard.lopez@inserm.fr.ORCID 0000-0001-5088-0155
Centre National de la Recherche Scientifique · FRInserm · FRUniversité Paris Cité · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells are inevitably challenged by low-level/endogenous stresses that do not arrest DNA replication. Here, in human primary cells, we discovered and characterized a noncanonical cellular response that is specific to nonblocking replication stress. Although this response generates reactive oxygen species (ROS), it induces a program that prevents the accumulation of premutagenic 8-oxoguanine in an adaptive way. Indeed, replication stress-induced ROS (RIR) activate FOXO1-controlled detoxification genes such as SEPP1, catalase, GPX1, and SOD2. Primary cells tightly control the production of RIR: They are excluded from the nucleus and are produced by the cellular NADPH oxidases DUOX1/DUOX2, whose expression is controlled by NF-κB, which is activated by PARP1 upon replication stress. In parallel, inflammatory cytokine gene expression is induced through the NF-κB-PARP1 axis upon nonblocking replication stress. Increasing replication stress intensity accumulates DNA double-strand breaks and triggers the suppression of RIR by p53 and ATM. These data underline the fine-tuning of the cellular response to stress that protects genome stability maintenance, showing that primary cells adapt their responses to replication stress severity.

Indexed as

NADPH OxidasesNF-kappa BCytokinesGenomic InstabilityHumansReactive Oxygen SpeciesCytokinesNADPH OxidasesNF-kappa BReactive Oxygen Species

Identifiers

PMID36869180
PMCPMC10154342
OpenAlexW4323048636

What OpenQuestion holds

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LicenceCC BY
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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.