Evidence map›Paper›PMID 37256941›Full record

ArticleScience advances2023

FIRRM/C1orf112 mediates resolution of homologous recombination intermediates in response to DNA interstrand crosslinks.

Abdelghani Mazouzi, Sarah C Moser, Federico Abascal, Bram van den Broek, Martin Del Castillo Velasco-Herrera, Ingrid van der Heijden, Maarten Hekkelman, Anne Paulien Drenth, Eline van der Burg, Lona J Kroese and 4 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. C1orf112 promotes breast cancer growth by modulating the cell cycle.Frontiers in bioengineering and biotechnology · 2026
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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

14 authors at 3 institutions in 2 countries.

Abdelghani MazouziDivision of Biochemistry, Netherlands Cancer Institute, Amsterdam, Netherlands.ORCID 0000-0003-0298-6304
Sarah C MoserOncode Institute, Amsterdam, Netherlands.ORCID 0000-0002-1678-4079
Federico AbascalSomatic Evolution, Wellcome Sanger Institute, Hinxton, UK.ORCID 0000-0002-6201-1587
Bram van den BroekDivision of Cell Biology, Netherlands Cancer Institute, Amsterdam, Netherlands.ORCID 0000-0003-1037-907X
Martin Del Castillo Velasco-HerreraExperimental Cancer Genetics, Wellcome Sanger Institute, Hinxton, UK.ORCID 0000-0001-5956-0211
Ingrid van der HeijdenOncode Institute, Amsterdam, Netherlands.ORCID 0000-0003-2849-8253
Maarten HekkelmanDivision of Biochemistry, Netherlands Cancer Institute, Amsterdam, Netherlands.ORCID 0000-0002-9081-4707
Anne Paulien DrenthOncode Institute, Amsterdam, Netherlands.
Eline van der BurgOncode Institute, Amsterdam, Netherlands.
Lona J KroeseAnimal Modeling Facility, Netherlands Cancer Institute, Amsterdam, Netherlands.
Kees JalinkDivision of Cell Biology, Netherlands Cancer Institute, Amsterdam, Netherlands.ORCID 0000-0001-7019-3440
David J AdamsExperimental Cancer Genetics, Wellcome Sanger Institute, Hinxton, UK.ORCID 0000-0001-9490-0306
Jos JonkersOncode Institute, Amsterdam, Netherlands.ORCID 0000-0002-9264-9792
Thijn R BrummelkampDivision of Biochemistry, Netherlands Cancer Institute, Amsterdam, Netherlands.ORCID 0000-0002-3066-7071
The Netherlands Cancer Institute · NLWellcome Sanger Institute · GBDutch Cancer Society · NL

Funding

Wellcome Trust
6 · The paper itself

Abstract

DNA interstrand crosslinks (ICLs) pose a major obstacle for DNA replication and transcription if left unrepaired. The cellular response to ICLs requires the coordination of various DNA repair mechanisms. Homologous recombination (HR) intermediates generated in response to ICLs, require efficient and timely conversion by structure-selective endonucleases. Our knowledge on the precise coordination of this process remains incomplete. Here, we designed complementary genetic screens to map the machinery involved in the response to ICLs and identified FIRRM/C1orf112 as an indispensable factor in maintaining genome stability. FIRRM deficiency leads to hypersensitivity to ICL-inducing compounds, accumulation of DNA damage during S-G

Indexed as

DNA DamageDNA RepairAnimalsDNADNA ReplicationHomologous RecombinationMiceDNA

Identifiers

PMID37256941
PMCPMC10413679
OpenAlexW4378894928

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.