Evidence map›Paper›PMID 31782600›Full record

ArticleEMBO reports2020

PHF6 promotes non-homologous end joining and G2 checkpoint recovery.

Daniël O Warmerdam, Ignacio Alonso-de Vega, Wouter W Wiegant, Bram van den Broek, Magdalena B Rother, Rob Mf Wolthuis, Raimundo Freire, Haico van Attikum, René H Medema, Veronique Aj Smits

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. PHF6 suppresses self-renewal of leukemic stem cells in AML.bioRxiv : the preprint server for biology · 2024
    Article
  7. Review
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  18. Frontiers in oncology · 2021
    Review
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  20. 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

10 authors at 4 institutions in 2 countries.

Daniël O WarmerdamCRISPR Platform, Cancer Center Amsterdam, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands.ORCID 0000-0003-1606-7448
Ignacio Alonso-de VegaUnidad de Investigación, Hospital Universitario de Canarias, La Laguna, Tenerife, Spain.
Wouter W WiegantDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Bram van den BroekDivision of Cell Biology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Magdalena B RotherDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.
Rob Mf WolthuisSection of Oncogenetics, Department of Clinical Genetics, Vrije Universiteit Amsterdam, Cancer Center Amsterdam, Amsterdam UMC, Amsterdam, The Netherlands.
Raimundo FreireUnidad de Investigación, Hospital Universitario de Canarias, La Laguna, Tenerife, Spain.
Haico van AttikumDepartment of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0001-8590-0240
René H MedemaDivision of Cell Biology, Oncode Institute, The Netherlands Cancer Institute, Amsterdam, The Netherlands.ORCID 0000-0002-6754-0381
Veronique Aj SmitsUnidad de Investigación, Hospital Universitario de Canarias, La Laguna, Tenerife, Spain.ORCID 0000-0002-9160-4525
Leiden University Medical Center · NLThe Netherlands Cancer Institute · NLUniversidad de La Laguna · ESAmsterdam University Medical Centers · NL

Funding

Agencia Canaria de Investigación, Innovación y Sociedad de la Información del Gobierno De Canarias TESIS2015010066Cancer Center AmsterdamMinisterio de Ciencia, Innovacion y Universidades BFU2017-90889-REDTMinisterio de Ciencia, Innovacion y Universidades SAF2016-80626Netherlands Organisation for Scientific Research VICI grant
6 · The paper itself

Abstract

The cellular response to DNA breaks is influenced by chromatin compaction. To identify chromatin regulators involved in the DNA damage response, we screened for genes that affect recovery following DNA damage using an RNAi library of chromatin regulators. We identified genes involved in chromatin remodeling, sister chromatid cohesion, and histone acetylation not previously associated with checkpoint recovery. Among these is the PHD finger protein 6 (PHF6), a gene mutated in Börjeson-Forssman-Lehmann syndrome and leukemic cancers. We find that loss of PHF6 dramatically compromises checkpoint recovery in G2 phase cells. Moreover, PHF6 is rapidly recruited to sites of DNA lesions in a PARP-dependent manner and required for efficient DNA repair through classical non-homologous end joining. These results indicate that PHF6 is a novel DNA damage response regulator that promotes end joining-mediated repair, thereby stimulating timely recovery from the G2 checkpoint.

Indexed as

HypogonadismX-Linked Intellectual DisabilityCell Line, TumorDNA End-Joining RepairG2 Phase Cell Cycle CheckpointsGrowth DisordersHumansRepressor ProteinsPHF6 protein, humanRepressor Proteinscheckpoint recoverychromatin regulatorsNHEJPHF6siRNA screen

Identifiers

PMID31782600
PMCPMC6944915
OpenAlexW2990628360

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.