Evidence map›Paper›PMID 32232336›Full record

ArticleNucleic acids research2020

PHF2 regulates homology-directed DNA repair by controlling the resection of DNA double strand breaks.

Ignacio Alonso-de Vega, Maria Cristina Paz-Cabrera, Magdalena B Rother, Wouter W Wiegant, Cintia Checa-Rodríguez, Juan Ramón Hernández-Fernaud, Pablo Huertas, Raimundo Freire, Haico van Attikum, Veronique A J Smits

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

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  18. JmjC Family of Histone Demethylases Form Nuclear Condensates.International journal of molecular sciences · 2022
    Article
  19. Review
  20. Frontiers in immunology · 2022
    Article
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

10 authors at 4 institutions in 2 countries.

Ignacio Alonso-de VegaUnidad de Investigación, Hospital Universitario de Canarias, Tenerife, Spain.
Maria Cristina Paz-CabreraUnidad de Investigación, Hospital Universitario de Canarias, Tenerife, Spain.
Magdalena B RotherDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Wouter W WiegantDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Cintia Checa-RodríguezCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Sevilla, Spain.
Juan Ramón Hernández-FernaudUnidad de Investigación, Hospital Universitario de Canarias, Tenerife, Spain.
Pablo HuertasCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Sevilla, Spain.
Raimundo FreireUnidad de Investigación, Hospital Universitario de Canarias, Tenerife, Spain.
Haico van AttikumDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Veronique A J SmitsUnidad de Investigación, Hospital Universitario de Canarias, Tenerife, Spain.
Hospital Universitario de Canarias · ESLeiden University Medical Center · NLCentro Andaluz de Biología Molecular y Medicina Regenerativa · ESUniversidad de La Laguna · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-translational histone modifications and chromatin remodelling play a critical role controlling the integrity of the genome. Here, we identify histone lysine demethylase PHF2 as a novel regulator of the DNA damage response by regulating DNA damage-induced focus formation of 53BP1 and BRCA1, critical factors in the pathway choice for DNA double strand break repair. PHF2 knockdown leads to impaired BRCA1 focus formation and delays the resolution of 53BP1 foci. Moreover, irradiation-induced RPA phosphorylation and focus formation, as well as localization of CtIP, required for DNA end resection, to sites of DNA lesions are affected by depletion of PHF2. These results are indicative of a defective resection of double strand breaks and thereby an impaired homologous recombination upon PHF2 depletion. In accordance with these data, Rad51 focus formation and homology-directed double strand break repair is inhibited in cells depleted for PHF2. Importantly, we demonstrate that PHF2 knockdown decreases CtIP and BRCA1 protein and mRNA levels, an effect that is dependent on the demethylase activity of PHF2. Furthermore, PHF2-depleted cells display genome instability and are mildly sensitive to the inhibition of PARP. Together these results demonstrate that PHF2 promotes DNA repair by homologous recombination by controlling CtIP-dependent resection of double strand breaks.

Indexed as

DNA Breaks, Double-StrandedRecombinational DNA RepairBRCA1 ProteinCell LineEndodeoxyribonucleasesGene Expression RegulationGenomic InstabilityHeLa CellsHistone DemethylasesHomeodomain ProteinsHumansBRCA1 ProteinEndodeoxyribonucleasesHistone DemethylasesHomeodomain ProteinsPHF2 protein, humanRBBP8 protein, human

Identifiers

PMID32232336
PMCPMC7229830
OpenAlexW3013579977

What OpenQuestion holds

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LicenceCC BY-NC
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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.