Evidence map›Paper›PMID 26584049›Full record

ArticlePLoS genetics2015

The Fanconi Anemia Pathway Protects Genome Integrity from R-loops.

María L García-Rubio, Carmen Pérez-Calero, Sonia I Barroso, Emanuela Tumini, Emilia Herrera-Moyano, Iván V Rosado, Andrés Aguilera

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed, 1 pooled it
13.3field-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

206 citing papers in PubMed, 1 synthesis or guideline pooled it, 312 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. MCM8-9 helicase activity protects primordial germ cell development to prevent premature ovarian insufficiency.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  13. Review
  14. Article
  15. Peroxiredoxin 1 safeguards the nucleolar genome from oxidative damage.bioRxiv : the preprint server for biology · 2025
    Article
  16. Article
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  18. Transcription-Replication Conflicts: Unlocking New Frontiers in Cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  19. Research square · 2025
    Article
  20. R-loops: a key driver of inflammatory responses in cancer.Experimental & molecular medicine · 2025
    Review

146 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 1 country.

María L García-RubioCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Seville, Spain.
Carmen Pérez-CaleroCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Seville, Spain.
Sonia I BarrosoCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Seville, Spain.
Emanuela TuminiCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Seville, Spain.
Emilia Herrera-MoyanoCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Seville, Spain.
Iván V RosadoInstituto de Biomedicina de Sevilla-Hospital Virgen del Rocío, Seville, Spain.
Andrés AguileraCentro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla, Seville, Spain.
Centro Andaluz de Biología Molecular y Medicina Regenerativa · ESUniversidad de Sevilla · ESInstituto de Biomedicina de Sevilla · ES

Funding

Worldwide Cancer Research 15-0098
6 · The paper itself

Abstract

Co-transcriptional RNA-DNA hybrids (R loops) cause genome instability. To prevent harmful R loop accumulation, cells have evolved specific eukaryotic factors, one being the BRCA2 double-strand break repair protein. As BRCA2 also protects stalled replication forks and is the FANCD1 member of the Fanconi Anemia (FA) pathway, we investigated the FA role in R loop-dependent genome instability. Using human and murine cells defective in FANCD2 or FANCA and primary bone marrow cells from FANCD2 deficient mice, we show that the FA pathway removes R loops, and that many DNA breaks accumulated in FA cells are R loop-dependent. Importantly, FANCD2 foci in untreated and MMC-treated cells are largely R loop dependent, suggesting that the FA functions at R loop-containing sites. We conclude that co-transcriptional R loops and R loop-mediated DNA damage greatly contribute to genome instability and that one major function of the FA pathway is to protect cells from R loops.

Indexed as

AnimalsBRCA2 ProteinDNADNA DamageDNA RepairDNA ReplicationFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinGenomic InstabilityHeLa CellsHumansMiceRNABRCA2 ProteinDNAFANCA protein, humanFANCD2 protein, humanFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinRNA

Identifiers

PMID26584049
PMCPMC4652862
OpenAlexW2207325914

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.