Evidence map›Paper›PMID 28572115›Full record

ArticleThe Journal of cell biology2017

Histone demethylase KDM5A regulates the ZMYND8-NuRD chromatin remodeler to promote DNA repair.

Fade Gong, Thomas Clouaire, Marion Aguirrebengoa, Gaëlle Legube, Kyle M Miller

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

115 citing papers in PubMed, 175 citations in OpenAlex.

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  17. Nucleoporins cooperate with Polycomb silencers to promote transcriptional repression and repair at DNA double-strand breaks.Proceedings of the National Academy of Sciences of the United States of America · 2025
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55 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

5 authors at 2 institutions in 2 countries.

Fade GongDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX.
Thomas ClouaireLaboratoire de Biologie Cellulaire et Moléculaire du Controle de la Prolifération, Centre de Biologie Intégrative, Centre National de la Recherche Scientifique, Université de Toulouse, Toulouse, France.
Marion AguirrebengoaLaboratoire de Biologie Cellulaire et Moléculaire du Controle de la Prolifération, Centre de Biologie Intégrative, Centre National de la Recherche Scientifique, Université de Toulouse, Toulouse, France.ORCID 0000-0001-5205-9774
Gaëlle LegubeLaboratoire de Biologie Cellulaire et Moléculaire du Controle de la Prolifération, Centre de Biologie Intégrative, Centre National de la Recherche Scientifique, Université de Toulouse, Toulouse, France.
Kyle M MillerDepartment of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX kyle.miller@austin.utexas.edu.ORCID 0000-0002-4544-0013
Université Fédérale de Toulouse Midi-Pyrénées · FRThe University of Texas at Austin · US

Funding

Shaping DNA Damage Response Networks Via Histone H2A VariantsR01CA198279 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI Kyle M Miller · 2016 to 2026
$3.3M
MECHANISMS OF GENOME MAINTENANCE BY BROMODOMAIN CHROMATIN READER PROTEINSR01CA201268 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI MILLER, KYLE M · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA198279NCI NIH HHS R01 CA201268
6 · The paper itself

Abstract

Upon DNA damage, histone modifications are dynamically reshaped to accommodate DNA damage signaling and repair within chromatin. In this study, we report the identification of the histone demethylase KDM5A as a key regulator of the bromodomain protein ZMYND8 and NuRD (nucleosome remodeling and histone deacetylation) complex in the DNA damage response. We observe KDM5A-dependent H3K4me3 demethylation within chromatin near DNA double-strand break (DSB) sites. Mechanistically, demethylation of H3K4me3 is required for ZMYND8-NuRD binding to chromatin and recruitment to DNA damage. Functionally, KDM5A deficiency results in impaired transcriptional silencing and repair of DSBs by homologous recombination. Thus, this study identifies a crucial function for KDM5A in demethylating H3K4 to allow ZMYND8-NuRD to operate within damaged chromatin to repair DSBs.

Indexed as

Chromatin Assembly and DisassemblyDNA Breaks, Double-StrandedRecombinational DNA RepairBinding SitesCell Line, TumorChromatinDealkylationDown-RegulationHEK293 CellsHistonesHumansMethylationMi-2 Nucleosome Remodeling and Deacetylase ComplexPoly(ADP-ribose) PolymerasesProtein BindingProtein Interaction Domains and MotifsChromatinHistonesKDM5A protein, humanMi-2 Nucleosome Remodeling and Deacetylase ComplexPoly(ADP-ribose) PolymerasesReceptors, Cell SurfaceReceptors for Activated C KinaseRetinoblastoma-Binding Protein 2Tumor Suppressor ProteinsZMYND8 protein, human

Identifiers

PMID28572115
PMCPMC5496618
OpenAlexW2621386467

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.