Evidence map›Paper›PMID 25365549›Full record

ReviewAntioxidants & redox signaling2015

Functional Crosstalk Between Lysine Methyltransferases on Histone Substrates: The Case of G9A/GLP and Polycomb Repressive Complex 2.

Chiara Mozzetta, Julien Pontis, Slimane Ait-Si-Ali

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  6. Review
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  9. Review
  10. Orchestration of H3K27 methylation: mechanisms and therapeutic implication.Cellular and molecular life sciences : CMLS · 2018
    Review
  11. Article
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  16. Review
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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.

Chiara MozzettaLaboratoire Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, Université Paris Diderot , Sorbonne Paris Cité, Paris, France .
Julien Pontis
Slimane Ait-Si-Ali
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

significanceMethylation of histone H3 on lysine 9 and 27 (H3K9 and H3K27) are two epigenetic modifications that have been linked to several crucial biological processes, among which are transcriptional silencing and cell differentiation. RECENT ADVANCES: Deposition of these marks is catalyzed by H3K9 lysine methyltransferases (KMTs) and polycomb repressive complex 2, respectively. Increasing evidence is emerging in favor of a functional crosstalk between these two major KMT families. CRITICAL ISSUES: Here, we review the current knowledge on the mechanisms of action and function of these enzymes, with particular emphasis on their interplay in the regulation of chromatin states and biological processes. We outline their crucial roles played in tissue homeostasis, by controlling the fate of embryonic and tissue-specific stem cells, highlighting how their deregulation is often linked to the emergence of a number of malignancies and neurological disorders. FUTURE DIRECTIONS: Histone methyltransferases are starting to be tested as drug targets. A new generation of highly selective chemical inhibitors is starting to emerge. These hold great promise for a rapid translation of targeting epigenetic drugs into clinical practice for a number of aggressive cancers and neurological disorders.

Indexed as

Histone-Lysine N-MethyltransferaseHistonesHumansPolycomb Repressive Complex 2Substrate SpecificityEHMT1 protein, humanHistone-Lysine N-MethyltransferaseHistonesPolycomb Repressive Complex 2

Identifiers

PMID25365549
PMCPMC4432786
OpenAlexW2108462555

What OpenQuestion holds

Textmetadata
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.