Evidence map›Paper›PMID 27612420›Full record

ArticleOncotarget2016

ATAD2 is an epigenetic reader of newly synthesized histone marks during DNA replication.

Seong Joo Koo, Amaury E Fernández-Montalván, Volker Badock, Christopher J Ott, Simon J Holton, Oliver von Ahsen, Joern Toedling, Sarah Vittori, James E Bradner, Mátyás Gorjánácz

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Genome-wide association study of mature cow size traits in American Angus cattle.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  13. ATAD2 Drives Prostate Cancer Progression to Metastasis.Molecular cancer research : MCR · 2025
    Article
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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 3 institutions in 2 countries.

Seong Joo KooDrug Discovery, Bayer Pharma AG, Berlin, Germany.
Amaury E Fernández-MontalvánDrug Discovery, Bayer Pharma AG, Berlin, Germany.
Volker BadockDrug Discovery, Bayer Pharma AG, Berlin, Germany.
Christopher J OttCenter for the Science of Therapeutics, Broad Institute, Cambridge, MA, USA.
Simon J HoltonDrug Discovery, Bayer Pharma AG, Berlin, Germany.
Oliver von AhsenDrug Discovery, Bayer Pharma AG, Berlin, Germany.
Joern ToedlingDrug Discovery, Bayer Pharma AG, Berlin, Germany.
Sarah VittoriCenter for the Science of Therapeutics, Broad Institute, Cambridge, MA, USA.
James E BradnerCenter for the Science of Therapeutics, Broad Institute, Cambridge, MA, USA.
Mátyás GorjánáczDrug Discovery, Bayer Pharma AG, Berlin, Germany.
Bayer (Germany) · DEHarvard University · USBroad Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATAD2 (ATPase family AAA domain-containing protein 2) is a chromatin regulator harboring an AAA+ ATPase domain and a bromodomain, previously proposed to function as an oncogenic transcription co-factor. Here we suggest that ATAD2 is also required for DNA replication. ATAD2 is co-expressed with genes involved in DNA replication in various cancer types and predominantly expressed in S phase cells where it localized on nascent chromatin (replication sites). Our extensive biochemical and cellular analyses revealed that ATAD2 is recruited to replication sites through a direct interaction with di-acetylated histone H4 at K5 and K12, indicative of newly synthesized histones during replication-coupled chromatin reassembly. Similar to ATAD2-depletion, ectopic expression of ATAD2 mutants that are deficient in binding to these di-acetylation marks resulted in reduced DNA replication and impaired loading of PCNA onto chromatin, suggesting relevance of ATAD2 in DNA replication. Taken together, our data show a novel function of ATAD2 in cancer and for the first time identify a reader of newly synthesized histone di-acetylation-marks during replication.

Indexed as

DNA ReplicationEpigenesis, GeneticHistone CodeAcetylationATPases Associated with Diverse Cellular ActivitiesDNA-Binding ProteinsHEK293 CellsHistone Deacetylase 1HistonesHumansATAD2 protein, humanATPases Associated with Diverse Cellular ActivitiesDNA-Binding ProteinsHDAC1 protein, humanHistone Deacetylase 1HistonesATAD2bromodomaincancerDNA replicationhistone acetylation

Identifiers

PMID27612420
PMCPMC5342555
OpenAlexW2520774405

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.