Evidence map›Paper›PMID 23112189›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Maintenance of gene silencing by the coordinate action of the H3K9 methyltransferase G9a/KMT1C and the H3K4 demethylase Jarid1a/KDM5A.

Chandra-Prakash Chaturvedi, Brinda Somasundaram, Kulwant Singh, Richard L Carpenedo, William L Stanford, F Jeffrey Dilworth, Marjorie Brand

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

50 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  6. Histone Methyltransferase G9a in Primary Sensory Neurons Promotes Inflammatory Pain and Transcription ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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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

7 authors at 2 institutions in 1 country.

Chandra-Prakash ChaturvediThe Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada K1H 8L6.
Brinda Somasundaram
Kulwant Singh
Richard L Carpenedo
William L Stanford
F Jeffrey Dilworth
Marjorie Brand
Ottawa Hospital · CAOttawa Hospital Research Institute

Funding

Canadian Institutes of Health Research MOP-77778Canadian Institutes of Health Research MOP-89834Canadian Institutes of Health Research MOP-89910
6 · The paper itself

Abstract

Chromatin remodeling is essential for controlling the expression of genes during development. The histone-modifying enzyme G9a/KMT1C can act both as a coactivator and a corepressor of transcription. Here, we show that the dual function of G9a as a coactivator vs. a corepressor entails its association within two distinct protein complexes, one containing the coactivator Mediator and one containing the corepressor Jarid1a/KDM5A. Functionally, G9a is important in stabilizing the Mediator complex for gene activation, whereas its repressive function entails a coordinate action with the histone H3 lysine 4 (H3K4) demethylase Jarid1a for the maintenance of gene repression. The essential nature of cross-talk between the histone methyltransferase G9a and the demethylase Jarid1a is demonstrated on the embryonic E(y)-globin gene, where the concurrent introduction of repressive histone marks (dimethylated H3K9 and dimethylated H3K27) and removal of activating histone mark (trimethylated H3K4) is required for maintenance of gene silencing. Taken together with our previous demonstration of cross-talk between UTX and MLL2 to mediate activation of the adult β(maj)-globin gene, these data suggest a model where "active" and "repressive" cross-talk between histone-modifying enzymes coexist on the same multigene locus and play a crucial role in the precise control of developmentally regulated gene expression.

Indexed as

AnimalsDNA-Binding ProteinsGene Expression Regulation, DevelopmentalGene SilencingGenetic LociGlobinsHistone DemethylasesHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesJumonji Domain-Containing Histone DemethylasesMediator ComplexMethylationMiceMice, KnockoutMyeloid-Lymphoid Leukemia ProteinDNA-Binding ProteinsGlobinsHistone DemethylasesHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesJumonji Domain-Containing Histone DemethylasesKdm5b protein, mouseKmt2d protein, mouseMediator ComplexMyeloid-Lymphoid Leukemia ProteinRetinoblastoma-Binding Protein 2Utx protein, mouse

Identifiers

PMID23112189
PMCPMC3503177
OpenAlexW2041941139

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.