Evidence map›Paper›PMID 33494958›Full record

ReviewTrends in genetics : TIG2021

Polycomb Gene Silencing Mechanisms: PRC2 Chromatin Targeting, H3K27me3 'Readout', and Phase Separation-Based Compaction.

Yiran Guo, Shuai Zhao, Gang Greg Wang

Open access · greenAbstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 1% 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

112 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

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  6. 3D chromatin structure remodelling in cancer.Cell communication and signaling : CCS · 2026
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52 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 at 1 institution in 1 country.

Yiran GuoLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Shuai ZhaoLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA.
Gang Greg WangLineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA; Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA; Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC 27599, USA. Electronic address: greg_wang@med.unc.edu.
University of North Carolina at Chapel Hill · US

Funding

Cancer Epigenetics: A novel PRC2 Dysregulation Mechanism in Multiple MyelomaR01CA211336 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, G GREG · 2017 to 2021
$2.0M
Determining the Role of DNA Methylation Deregulation in OncogenesisR01CA215284 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WANG, G GREG · 2017 to 2021
$1.7M
NCI NIH HHS R01 CA211336NCI NIH HHS R01 CA215284
6 · The paper itself

Abstract

Modulation of chromatin structure and/or modification by Polycomb repressive complexes (PRCs) provides an important means to partition the genome into functionally distinct subdomains and to regulate the activity of the underlying genes. Both the enzymatic activity of PRC2 and its chromatin recruitment, spreading, and eviction are exquisitely regulated via interactions with cofactors and DNA elements (such as unmethylated CpG islands), histones, RNA (nascent mRNA and long noncoding RNA), and R-loops. PRC2-catalyzed histone H3 lysine 27 trimethylation (H3K27me3) is recognized by distinct classes of effectors such as canonical PRC1 and BAH module-containing proteins (notably BAHCC1 in human). These effectors mediate gene silencing by different mechanisms including phase separation-related chromatin compaction and histone deacetylation. We discuss recent advances in understanding the structural architecture of PRC2, the regulation of its activity and chromatin recruitment, and the molecular mechanisms underlying Polycomb-mediated gene silencing. Because PRC deregulation is intimately associated with the development of diseases, a better appreciation of Polycomb-based (epi)genomic regulation will have far-reaching implications in biology and medicine.

Indexed as

AlkynesAnimalsChromatinGene SilencingHistonesHumansLysinePolycomb Repressive Complex 2RNA, Long NoncodingVertebratesAlkynesChromatinHistonesLysinemethylacetylenePolycomb Repressive Complex 2RNA, Long Noncodingallosteric activationBAHchromatinchromodomainCpG islandH3K27me3histonemethylationphase separationPolycombPRC1PRC2R-loopRNAtranscription

Identifiers

PMID33494958
PMCPMC8119337
OpenAlexW3125269882

What OpenQuestion holds

Textmetadata
LicenceTDM
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.