Evidence map›Paper›PMID 30804473›Full record

ArticleCell death and differentiation2019

ING3 is required for ATM signaling and DNA repair in response to DNA double strand breaks.

Audrey Mouche, Jérôme Archambeau, Charles Ricordel, Laura Chaillot, Nicolas Bigot, Thierry Guillaudeux, Muriel Grenon, Rémy Pedeux

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

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  9. Overexpression ofExperimental and therapeutic medicine · 2021
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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

8 authors at 2 institutions in 3 countries.

Audrey MoucheINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, Rennes, France.
Jérôme ArchambeauINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, Rennes, France.
Charles RicordelINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, Rennes, France.
Laura ChaillotINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, Rennes, France.
Nicolas BigotUniversité de Rennes 1, Rennes, France.
Thierry GuillaudeuxINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, Rennes, France.
Muriel GrenonBiochemistry, School of Natural Sciences, National University of Ireland, Galway, Ireland.ORCID http://orcid.org/0000-0002-9910-5974
Rémy PedeuxINSERM U1242, Chemistry Oncogenesis Stress and Signaling, CLCC Eugène Marquis, Rennes, France. remy.pedeux@univ-rennes1.fr.
Inserm · FROllscoil na Gaillimhe – University of Galway · IE

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-11-RPIB-0012
6 · The paper itself

Abstract

Inhibitor of Growth 3 (ING3) is a candidate tumor suppressor gene whose expression is lost in tumors such as hepatocellular carcinoma, head and neck squamous cell carcinoma and melanoma. In the present study, we show that ING3-depleted human cells and yeast cells deleted for its ortholog YNG2 are sensitive to DNA damage suggesting a conserved role in response to such stress. In human cells, ING3 is recruited to DNA double strand breaks and is required for ATM activation. Remarkably, in response to doxorubicin, ATM activation is dependent on ING3 but not on TIP60, whose recruitment to DNA breaks also depends on ING3. These events lead to ATM-mediated phosphorylation of NBS1 and the subsequent recruitment of RNF8, RNF168, 53BP1, and BRCA1, which are major mediators of the DNA damage response. Accordingly, upon genotoxic stress, DNA repair by non-homologous end joining (NHEJ) or homologous recombination (HR) were impaired in absence of ING3. Finally, immunoglobulin class switch recombination (CSR), a physiological mechanism requiring NHEJ repair, was impaired in the absence of ING3. Since deregulation of DNA double strand break repair is associated with genomic instability, we propose a novel function of ING3 as a caretaker tumor suppressor involved in the DNA damage signaling and repair.

Indexed as

A549 CellsAcetyltransferasesAnimalsAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCell Line, TumorDNADNA-Binding ProteinsDNA Breaks, Double-StrandedDNA End-Joining RepairDoxorubicinEnzyme ActivationGenomic InstabilityHomeodomain ProteinsHumansAcetyltransferasesAntibiotics, AntineoplasticAtaxia Telangiectasia Mutated ProteinsATM protein, humanBRCA1 ProteinBRCA1 protein, humanDNADNA-Binding ProteinsDoxorubicinHomeodomain ProteinsING3 protein, humanKAT5 protein, humanLysine Acetyltransferase 5RNA, Small InterferingRNF168 protein, humanRNF8 protein, humanSaccharomyces cerevisiae ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1Tumor Suppressor ProteinsUbiquitin-Protein LigasesYng2 protein, S cerevisiae

Identifiers

PMID30804473
PMCPMC6889383
OpenAlexW2916000762

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.