Evidence map›Paper›PMID 26675384›Full record

ReviewTrends in genetics : TIG2016

H3K9me3-Dependent Heterochromatin: Barrier to Cell Fate Changes.

Justin S Becker, Dario Nicetto, Kenneth S Zaret

Abstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 286 papers.

0numbers the graph read from it
0cells of the map it votes in
286citing 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

286 citing papers in PubMed.

  1. Article
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  4. AlphaGenome Atlas:medRxiv : the preprint server for health sciences · 2026
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  19. Liquid-liquid phase separation in neural development.Cellular and molecular life sciences : CMLS · 2026
    Review
  20. Article

226 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

3 authors.

Justin S BeckerInstitute for Regenerative Medicine, Epigenetics Program, and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Dario NicettoInstitute for Regenerative Medicine, Epigenetics Program, and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA.
Kenneth S ZaretInstitute for Regenerative Medicine, Epigenetics Program, and Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Smilow Center for Translational Research, 3400 Civic Center Boulevard, Philadelphia, PA 19104, USA. Electronic address: zaret@upenn.edu.

Funding

Roles of sumoylation and alternative polyadenylation in cellular reprogrammingP01GM099134 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HOCHEDLINGER, KONRAD · 2011 to 2021
$20.3M
TRANS-ACTING FACTORS CAUSING CELL-SPECIFIC GENE CONTROLR01GM036477 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI ZARET, KENNETH · 1986 to 2023
$7.7M
Unlocking heterochromatin to potentiate cell conversion to the hepatocyte fateF31DK107183 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BECKER, JUSTIN SCOTT · 2015 to 2016
$41k
NIDDK NIH HHS F31 DK107183NIGMS NIH HHS P01 GM099134NIGMS NIH HHS R01 GM036477
6 · The paper itself

Abstract

Establishing and maintaining cell identity depends on the proper regulation of gene expression, as specified by transcription factors and reinforced by epigenetic mechanisms. Among the epigenetic mechanisms, heterochromatin formation is crucial for the preservation of genome stability and the cell type-specific silencing of genes. The heterochromatin-associated histone mark H3K9me3, although traditionally associated with the noncoding portions of the genome, has emerged as a key player in repressing lineage-inappropriate genes and shielding them from activation by transcription factors. Here we describe the role of H3K9me3 heterochromatin in impeding the reprogramming of cell identity and the mechanisms by which H3K9me3 is reorganized during development and cell fate determination.

Indexed as

Cellular ReprogrammingGene SilencingAnimalsCell DifferentiationEpigenesis, GeneticGene Expression Regulation, DevelopmentalHeterochromatinHistonesHumansPluripotent Stem CellsTranscription FactorsHeterochromatinHistonesTranscription Factorscell identitydevelopmentH3K9me3heterochromatinreprogramming

Identifiers

PMID26675384
PMCPMC4698194

What OpenQuestion holds

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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.