Evidence map›Paper›PMID 31858687›Full record

ArticleAging cell2020

Hdac3, Setdb1, and Kap1 mark H3K9me3/H3K14ac bivalent regions in young and aged liver.

Andrew J Price, Mohan C Manjegowda, Jessica Kain, Swetha Anandh, Irina M Bochkis

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The Many Faces of SetDB1.Epigenomes · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Sequential ChIP-Seq.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  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

5 authors at 1 institution in 1 country.

Andrew J PriceDepartment of Pharmacology, University of Virginia, Charlottesville, VA, USA.
Mohan C ManjegowdaDepartment of Pharmacology, University of Virginia, Charlottesville, VA, USA.
Jessica KainDepartment of Pharmacology, University of Virginia, Charlottesville, VA, USA.
Swetha AnandhDepartment of Pharmacology, University of Virginia, Charlottesville, VA, USA.
Irina M BochkisDepartment of Pharmacology, University of Virginia, Charlottesville, VA, USA.ORCID 0000-0001-8073-8408
University of Virginia · US

Funding

Nucleosome architecture in aging and nuclear receptor activation in the liverK01DK101633 · NIDDK · UNIVERSITY OF VIRGINIA · PI BOCHKIS, IRINA · 2014 to 2018
$701k
NIDDK NIH HHS DK-101633NIDDK NIH HHS K01 DK101633
6 · The paper itself

Abstract

Post-translational modifications of histone tails play a crucial role in gene regulation. Here, we performed chromatin profiling by quantitative targeted mass spectrometry to assess all possible modifications of the core histones. We identified a bivalent combination, a dually marked H3K9me3/H3K14ac modification in the liver, that is significantly decreased in old hepatocytes. Subsequent sequential ChIP-Seq identified dually marked single nucleosome regions, with reduced number of sites and decreased signal in old livers, confirming mass spectrometry results. We detected H3K9me3 and H3K14ac bulk ChIP-Seq signal in reChIP nucleosome regions, suggesting a correlation between H3K9me3/H3K14ac bulk bivalent genomic regions and dually marked single nucleosomes. Histone H3K9 deacetylase Hdac3, as well as H3K9 methyltransferase Setdb1, found in complex Kap1, occupied both bulk and single nucleosome bivalent regions in both young and old livers, correlating to presence of H3K9me3. Expression of genes associated with bivalent regions in young liver, including those regulating cholesterol secretion and triglyceride synthesis, is upregulated in old liver once the bivalency is lost. Hence, H3K9me3/H3K14ac dually marked regions define a poised inactive state that is resolved with loss of one or both of the chromatin marks, which subsequently leads to change in gene expression.

Indexed as

AcetylationAgingAnimalsChromatinChromatin Immunoprecipitation SequencingHistone Deacetylase 3Histone DeacetylasesHistone-Lysine N-MethyltransferaseHistonesLipid MetabolismLiverMaleMass SpectrometryMethylationMiceMice, Inbred C57BLChromatinHistone Deacetylase 3Histone DeacetylasesHistone-Lysine N-MethyltransferaseHistonesNucleosomesProteomeSETDB1 protein, mouseTrim28 protein, mouseTripartite Motif-Containing Protein 28bivalent domainchromatin remodelingHdac3Kap1lipid metabolismliverSetdb1

Identifiers

PMID31858687
PMCPMC6996956
OpenAlexW2995418626

What OpenQuestion holds

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LicenceCC BY
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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.