Evidence map›Paper›PMID 29590434›Full record

ArticleNucleic acids research2018

An E2F7-dependent transcriptional program modulates DNA damage repair and genomic stability.

Jone Mitxelena, Aintzane Apraiz, Jon Vallejo-Rodríguez, Iraia García-Santisteban, Asier Fullaondo, Mónica Alvarez-Fernández, Marcos Malumbres, Ana M Zubiaga

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. Exploring gastric cancer genetics: A turning point in common variable immunodeficiency.The journal of allergy and clinical immunology. Global · 2024
    Article
  9. Article
  10. Expression profiling of luminal B breast tumor in Indian women.Journal of cancer research and clinical oncology · 2023
    Article
  11. E2F7 drives autotaxin/Enpp2 transcription via chromosome looping: Repression by p53 in murine but not in human carcinomas.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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  12. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Jone MitxelenaDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country UPV/EHU, 48080 Bilbao, Spain.
Aintzane ApraizDepartment of Cell Biology and Histology, University of the Basque Country UPV/EHU, 48080 Bilbao, Spain.
Jon Vallejo-RodríguezDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country UPV/EHU, 48080 Bilbao, Spain.
Iraia García-SantistebanDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country UPV/EHU, 48080 Bilbao, Spain.
Asier FullaondoDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country UPV/EHU, 48080 Bilbao, Spain.
Mónica Alvarez-FernándezCell Division and Cancer Group, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Marcos MalumbresCell Division and Cancer Group, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Ana M ZubiagaDepartment of Genetics, Physical Anthropology and Animal Physiology, University of the Basque Country UPV/EHU, 48080 Bilbao, Spain.
University of the Basque Country · ESSpanish National Cancer Research Centre · ES

Funding

Worldwide Cancer Research 15-0278
6 · The paper itself

Abstract

The cellular response to DNA damage is essential for maintaining the integrity of the genome. Recent evidence has identified E2F7 as a key player in DNA damage-dependent transcriptional regulation of cell-cycle genes. However, the contribution of E2F7 to cellular responses upon genotoxic damage is still poorly defined. Here we show that E2F7 represses the expression of genes involved in the maintenance of genomic stability, both throughout the cell cycle and upon induction of DNA lesions that interfere with replication fork progression. Knockdown of E2F7 leads to a reduction in 53BP1 and FANCD2 foci and to fewer chromosomal aberrations following treatment with agents that cause interstrand crosslink (ICL) lesions but not upon ionizing radiation. Accordingly, E2F7-depleted cells exhibit enhanced cell-cycle re-entry and clonogenic survival after exposure to ICL-inducing agents. We further report that expression and functional activity of E2F7 are p53-independent in this context. Using a cell-based assay, we show that E2F7 restricts homologous recombination through the transcriptional repression of RAD51. Finally, we present evidence that downregulation of E2F7 confers an increased resistance to chemotherapy in recombination-deficient cells. Taken together, our results reveal an E2F7-dependent transcriptional program that contributes to the regulation of DNA repair and genomic integrity.

Indexed as

DNA RepairGene Expression RegulationGenomic InstabilityCell CycleCell LineChromosome BreakageDNA DamageE2F7 Transcription FactorHumansPromoter Regions, GeneticRecombinational DNA RepairTranscription, GeneticTranscriptomeTumor Suppressor Protein p53E2F7 protein, humanE2F7 Transcription FactorTumor Suppressor Protein p53

Identifiers

PMID29590434
PMCPMC5961008
OpenAlexW2790279422

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.