Evidence map›Paper›PMID 23990607›Full record

ArticleGenome research2013

H4K16 acetylation marks active genes and enhancers of embryonic stem cells, but does not alter chromatin compaction.

Gillian C A Taylor, Ragnhild Eskeland, Betül Hekimoglu-Balkan, Madapura M Pradeepa, Wendy A Bickmore

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
–field-weighted citation impact
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

125 citing papers in PubMed, 198 citations in OpenAlex.

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  13. Basic Epigenetic Mechanisms.Sub-cellular biochemistry · 2025
    Review
  14. Review
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  20. Article

65 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 1 institution in 1 country.

Gillian C A TaylorMRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine at University of Edinburgh, Edinburgh EH4 2XU, United Kingdom.
Ragnhild Eskeland
Betül Hekimoglu-Balkan
Madapura M Pradeepa
Wendy A Bickmore
Institute of Genetics and Cancer · GB

Funding

Medical Research CouncilWellcome Trust
6 · The paper itself

Abstract

Compared with histone H3, acetylation of H4 tails has not been well studied, especially in mammalian cells. Yet, H4K16 acetylation is of particular interest because of its ability to decompact nucleosomes in vitro and its involvement in dosage compensation in flies. Here we show that, surprisingly, loss of H4K16 acetylation does not alter higher-order chromatin compaction in vivo in mouse embryonic stem cells (ESCs). As well as peaks of acetylated H4K16 and KAT8 histone acetyltransferase at the transcription start sites of expressed genes, we report that acetylation of H4K16 is a new marker of active enhancers in ESCs and that some enhancers are marked by H3K4me1, KAT8, and H4K16ac, but not by acetylated H3K27 or EP300, suggesting that they are novel EP300 independent regulatory elements. Our data suggest a broad role for different histone acetylation marks and for different histone acetyltransferases in long-range gene regulation.

Indexed as

Enhancer Elements, GeneticAcetylationAnimalsCells, CulturedChromatinDosage Compensation, GeneticE1A-Associated p300 ProteinEmbryonic Stem CellsEpigenesis, GeneticGene Expression ProfilingGene Expression Regulation, DevelopmentalHistone AcetyltransferasesHistonesIn Situ Hybridization, FluorescenceMiceOligonucleotide Array Sequence AnalysisChromatinE1A-Associated p300 ProteinHistone AcetyltransferasesHistones

Identifiers

PMID23990607
PMCPMC3847775
OpenAlexW2153093716

What OpenQuestion holds

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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.