Evidence map›Paper›PMID 37832547›Full record

ArticleMolecular cell2023

DNA damage induces nuclear envelope rupture through ATR-mediated phosphorylation of lamin A/C.

Marton Tibor Kovacs, Marie Vallette, Pauline Wiertsema, Florent Dingli, Damarys Loew, Guilherme Pedreira de Freitas Nader, Matthieu Piel, Raphael Ceccaldi

Open access · hybridAbstract read
In one paragraph

Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

55 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
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  6. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
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  14. ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Marton Tibor KovacsInserm U830, PSL Research University, Institut Curie, 75005 Paris, France.
Marie ValletteInserm U830, PSL Research University, Institut Curie, 75005 Paris, France.
Pauline WiertsemaInserm U830, PSL Research University, Institut Curie, 75005 Paris, France.
Florent DingliInstitut Curie, PSL Research University, Centre de Recherche, CurieCoreTech Spectrométrie de Masse Protéomique, 26 rue d'Ulm, Paris 75248 Cedex 05, France.
Damarys LoewInstitut Curie, PSL Research University, Centre de Recherche, CurieCoreTech Spectrométrie de Masse Protéomique, 26 rue d'Ulm, Paris 75248 Cedex 05, France.
Guilherme Pedreira de Freitas NaderInstitut Curie and Institut Pierre Gilles de Gennes, PSL Research University, CNRS, UMR 144, Paris, France.
Matthieu PielInstitut Curie and Institut Pierre Gilles de Gennes, PSL Research University, CNRS, UMR 144, Paris, France.
Raphael CeccaldiInserm U830, PSL Research University, Institut Curie, 75005 Paris, France. Electronic address: raphael.ceccaldi@curie.fr.
Inserm · FRCentre National de la Recherche Scientifique · FRUniversité Paris Sciences et Lettres · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The integrity of the nuclear envelope (NE) is essential for maintaining the structural stability of the nucleus. Rupture of the NE has been frequently observed in cancer cells, especially in the context of mechanical challenges, such as physical confinement and migration. However, spontaneous NE rupture events, without any obvious physical challenges to the cell, have also been described. The molecular mechanism(s) of these spontaneous NE rupture events remain to be explored. Here, we show that DNA damage and subsequent ATR activation leads to NE rupture. Upon DNA damage, lamin A/C is phosphorylated in an ATR-dependent manner, leading to changes in lamina assembly and, ultimately, NE rupture. In addition, we show that cancer cells with intrinsic DNA repair defects undergo frequent events of DNA-damage-induced NE rupture, which renders them extremely sensitive to further NE perturbations. Exploiting this NE vulnerability could provide a new angle to complement traditional, DNA-damage-based chemotherapy.

Indexed as

Lamin Type ANuclear EnvelopeCell NucleusDNADNA DamagePhosphorylationDNALamin Type AATRDNA damagehomologous recombination deficiencylaminalamin A/C phosphorylationNE vulnerabilitynuclear envelope rupturereplication stresssynthetic lethality

Identifiers

PMID37832547
PMCPMC10597398
OpenAlexW4387570527

What OpenQuestion holds

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LicenceCC BY-NC
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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.