Evidence map›Paper›PMID 40615546›Full record

ArticleCommunications biology2025

TopBP1 coordinates DNA repair synthesis in mitosis via recruitment of the nuclease scaffold SLX4.

Jonas Bagge, Kamilla Vandsø Petersen, Sinem N Karakus, Thorbjørn M Nielsen, Johanne Rask, Christian R Brøgger, Jonas Jensen, Meliti Skouteri, Antony M Carr, Ivo A Hendriks and 2 more

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
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  6. 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

12 authors.

Jonas Bagge *Section for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.ORCID http://orcid.org/0000-0002-0884-5337
Kamilla Vandsø Petersen *Section for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.
Sinem N KarakusSection for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.
Thorbjørn M NielsenSection for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.ORCID http://orcid.org/0000-0003-4002-8027
Johanne RaskSection for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.
Christian R BrøggerSection for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.
Jonas JensenSection for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.
Meliti SkouteriGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton, UK.
Antony M CarrGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton, UK.ORCID http://orcid.org/0000-0002-2028-2389
Ivo A HendriksNovo Nordisk Foundation Center for Protein Research, University of Copenhagen, Copenhagen N, Denmark.ORCID http://orcid.org/0000-0002-1439-3701
Vibe H OestergaardSection for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark.ORCID http://orcid.org/0000-0002-1633-0560
Michael LisbySection for Functional Genomics, Department of Biology, University of Copenhagen, Copenhagen N, Denmark. mlisby@bio.ku.dk.ORCID http://orcid.org/0000-0002-4830-5247

Funding

Carlsbergfondet (Carlsberg Foundation) CF22-0494Kræftens Bekæmpelse (Danish Cancer Society) R325-A18939Novo Nordisk Fonden (Novo Nordisk Foundation) NAVillum Fonden (Villum Foundation) NA
6 · The paper itself

Abstract

The majority of cancer cells experience replication stress, which ultimately causes them to enter mitosis with underreplicated DNA. To alleviate the consequences of replication stress, cells utilize a mechanism known as MiDAS that functions to complete synthesis of underreplicated DNA in early mitosis. This process is considered an Achilles heel for highly replicative cancers. In this study, we show that human TopBP1 localizes to sites of underreplicated DNA marked by FANCD2 and promotes MiDAS through recruitment of the nuclease scaffold protein SLX4. Additionally, we demonstrate that the recruitment of SLX4 to TopBP1 foci in mitosis depends on TopBP1-K704, SLX4-T1260, and several SUMO-interaction motifs in SLX4. Lastly, we show that the recruitment of SLX4 to TopBP1 foci in mitosis is important to prevent transmission of DNA damage to daughter cells. Based on this, we hypothesize that targeting the TopBP1-SLX4 interaction in mitosis may be a potential strategy for anti-cancer therapy.

Indexed as

Carrier ProteinsDNA-Binding ProteinsDNA RepairMitosisNuclear ProteinsRecombinasesDNA DamageDNA ReplicationHeLa CellsHumansCarrier ProteinsDNA-Binding ProteinsNuclear ProteinsRecombinasesSLX4 protein, humanTOPBP1 protein, human

Identifiers

PMID40615546
PMCPMC12227572

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.