Evidence map›Paper›PMID 34400841›Full record

ReviewNature reviews. Molecular cell biology2021

The molecular principles of gene regulation by Polycomb repressive complexes.

Neil P Blackledge, Robert J Klose

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Molecular cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 305 papers.

0numbers the graph read from it
0cells of the map it votes in
305citing papers in PubMed
28.6field-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

305 citing papers in PubMed, 487 citations in OpenAlex.

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245 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

2 authors at 1 institution in 1 country.

Neil P BlackledgeDepartment of Biochemistry, University of Oxford, Oxford, UK. neil.blackledge@bioch.ox.ac.uk.
Robert J KloseDepartment of Biochemistry, University of Oxford, Oxford, UK. rob.klose@bioch.ox.ac.uk.ORCID 0000-0002-8726-7888
University of Oxford · GB

Funding

Wellcome Trust 209400
6 · The paper itself

Abstract

Precise control of gene expression is fundamental to cell function and development. Although ultimately gene expression relies on DNA-binding transcription factors to guide the activity of the transcription machinery to genes, it has also become clear that chromatin and histone post-translational modification have fundamental roles in gene regulation. Polycomb repressive complexes represent a paradigm of chromatin-based gene regulation in animals. The Polycomb repressive system comprises two central protein complexes, Polycomb repressive complex 1 (PRC1) and PRC2, which are essential for normal gene regulation and development. Our early understanding of Polycomb function relied on studies in simple model organisms, but more recently it has become apparent that this system has expanded and diverged in mammals. Detailed studies are now uncovering the molecular mechanisms that enable mammalian PRC1 and PRC2 to identify their target sites in the genome, communicate through feedback mechanisms to create Polycomb chromatin domains and control transcription to regulate gene expression. In this Review, we discuss and contextualize the emerging principles that define how this fascinating chromatin-based system regulates gene expression in mammals.

Indexed as

ChromatinGene Expression RegulationHistonesHumansMethylationPolycomb Repressive Complex 1Polycomb Repressive Complex 2Protein Processing, Post-TranslationalTranscription, GeneticUbiquitinationChromatinHistonesPolycomb Repressive Complex 1Polycomb Repressive Complex 2

Identifiers

PMID34400841
PMCPMC7612013
OpenAlexW3193447048

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.