Evidence map›Paper›PMID 40717024›Full record

ReviewThe FEBS journal2026

Chromatin folding by the Polycomb group proteins and its elusive role in epigenetic repression.

Ludvig Lizana, Yuri B Schwartz

Abstract readReview
In one paragraph

Review in The FEBS journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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

2 authors.

Ludvig LizanaIntegrated Science Lab, Department of Physics, Umeå University, Umeå, Sweden.
Yuri B SchwartzEpigenetic Cooperation North (EpiCoN), Umeå University, Umeå, Sweden.ORCID 0000-0003-4790-3920

Funding

Cancerfonden 22 2285 PjInsamlingsstiftelsenKempestiftelserna JCK22-0055Medical Faculty, Umeå UniversityVetenskapsrådet 2021-04080Vetenskapsrådet 2021-04435
6 · The paper itself

Abstract

The Polycomb system epigenetically represses selected developmental genes to enforce gene expression programs of differentiated cells. The system requires the coordinated action of dozens of structurally unrelated proteins assembled in two evolutionarily conserved polycomb repressive complexes, PRC1 and PRC2. Genes repressed by the Polycomb system are enriched in histone H3 trimethylated at lysine 27 (H3K27me3), an epigenetic mark that propagates the repressed state after DNA replication. Despite the impressive progress in dissecting molecular functions of the Polycomb group proteins, the fundamental questions of how the Polycomb system represses transcription or how the H3K27me3 mark is translated to benefit the repression are still open. Multiple observations indicate that the binding of PRC1, PRC2, and elevated H3K27me3 correlate with changes in the chromatin structure of target genes, which may be integral for the associated epigenetic repression. In this Review, we summarize our current understanding of these observations. We discuss the chromatin folding inside the loci repressed by the Polycomb system, consider molecular processes causing it and reflect upon its possible impact on transcription and epigenetic memory of the repressed state.

Indexed as

ChromatinEpigenesis, GeneticEpigenetic RepressionPolycomb-Group ProteinsAnimalsHistonesHumansChromatinHistonesPolycomb-Group Proteinschromatincomputational modellingepigeneticsgenome architecturePolycombtranscriptional repression

Identifiers

PMID40717024
PMCPMC12797019

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.