Evidence map›Paper›PMID 34452908›Full record

ArticleScience advances2021

Lamin B1 sequesters 53BP1 to control its recruitment to DNA damage.

Laure Etourneaud, Angela Moussa, Emilie Rass, Diane Genet, Simon Willaume, Caroline Chabance-Okumura, Paul Wanschoor, Julien Picotto, Benoît Thézé, Jordane Dépagne and 12 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 49 citations in OpenAlex.

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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

22 authors at 4 institutions in 2 countries.

Laure EtourneaudUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0003-3938-7559
Angela MoussaUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0002-0970-0885
Emilie RassUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0003-4890-7771
Diane GenetUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0001-8983-3794
Simon WillaumeUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0003-3249-8272
Caroline Chabance-OkumuraUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Paul WanschoorUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Julien PicottoUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Benoît ThézéUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0002-0146-0354
Jordane DépagneGenetic Engineering and Expression Platform (CIGEX), iRCM, DRF, CEA, Fontenay-aux-Roses, France.
Xavier VeauteGenetic Engineering and Expression Platform (CIGEX), iRCM, DRF, CEA, Fontenay-aux-Roses, France.
Eléa DizetGenetic Engineering and Expression Platform (CIGEX), iRCM, DRF, CEA, Fontenay-aux-Roses, France.
Didier BussoGenetic Engineering and Expression Platform (CIGEX), iRCM, DRF, CEA, Fontenay-aux-Roses, France.ORCID 0000-0003-3027-7900
Aurélia BarascuUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Lamya IrbahUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Thierry KortulewskiUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Anna CampalansUniversité de Paris and Université Paris Saclay, iRCM/IBFJ, CEA, UMR Stabilité Génétique Cellules Souches et Radiations, "Genetic Instability Research" Team, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0001-7089-6891
Catherine Le ChalonyUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Sophie Zinn-JustinLaboratory of Structural Biology and Radiobiology, Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Université Paris-Saclay, F-91190 Gif-sur-Yvette, France.
Ralph ScullyDepartment of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Gaëlle PennarunUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France.
Pascale BertrandUniversité de Paris and Université Paris Saclay, INSERM, iRCM/IBFJ, CEA, UMR Stabilité Génétique, Cellules Souches et Radiations, F-92265 Fontenay-aux-Roses, France. pascale.bertrand@cea.fr.ORCID 0000-0002-9019-742X
Inserm · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRBeth Israel Deaconess Medical Center · USCentre National de la Recherche Scientifique · FR

Funding

ANALYSIS OF BRCA1 RECOMBINATION FUNCTIONSR01CA095175 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SCULLY, RALPH · 2002 to 2021
$4.9M
NCI NIH HHS R01 CA095175
6 · The paper itself

Abstract

Double-strand breaks (DSBs) are harmful lesions and a major cause of genome instability. Studies have suggested a link between the nuclear envelope and the DNA damage response. Here, we show that lamin B1, a major component of the nuclear envelope, interacts directly with 53BP1 protein, which plays a pivotal role in the DSB repair. This interaction is dissociated after DNA damage. Lamin B1 overexpression impedes 53BP1 recruitment to DNA damage sites and leads to a persistence of DNA damage, a defect in nonhomologous end joining and an increased sensitivity to DSBs. The identification of interactions domains between lamin B1 and 53BP1 allows us to demonstrate that the defect of 53BP1 recruitment and the DSB persistence upon lamin B1 overexpression are due to sequestration of 53BP1 by lamin B1. This study highlights lamin B1 as a factor controlling the recruitment of 53BP1 to DNA damage sites upon injury.

Indexed as

DNA Breaks, Double-StrandedLamin Type BDNA DamageDNA End-Joining RepairTumor Suppressor p53-Binding Protein 1Lamin Type BTumor Suppressor p53-Binding Protein 1

Identifiers

PMID34452908
PMCPMC8397269
OpenAlexW3194798061

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.