Evidence map›Paper›PMID 23353889›Full record

ArticleThe EMBO journal2013

TET2 and TET3 regulate GlcNAcylation and H3K4 methylation through OGT and SET1/COMPASS.

Rachel Deplus, Benjamin Delatte, Marie K Schwinn, Matthieu Defrance, Jacqui Méndez, Nancy Murphy, Mark A Dawson, Michael Volkmar, Pascale Putmans, Emilie Calonne and 8 more

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 326 papers.

0numbers the graph read from it
0cells of the map it votes in
326citing papers in PubMed
27.4field-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

326 citing papers in PubMed, 486 citations in OpenAlex.

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  7. Maternal O-GlcNAc Transferase Is Required for the Asymmetry of Epigenetic Modifications in Mouse Zygotes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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266 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 7 institutions in 4 countries.

Rachel DeplusLaboratory of Cancer Epigenetics, Faculty of Medicine, Université Libre de Bruxelles, Brussels, Belgium.
Benjamin Delatte
Marie K Schwinn
Matthieu Defrance
Jacqui Méndez
Nancy Murphy
Mark A Dawson
Michael Volkmar
Pascale Putmans
Emilie Calonne
Alan H Shih
Ross L Levine
Olivier Bernard
Thomas Mercher
Eric Solary
Marjeta Urh
Danette L Daniels
François Fuks
Université Libre de Bruxelles · BEPromega (United States) · USMemorial Sloan Kettering Cancer Center · USInserm · FRInstitut Gustave Roussy · FRUniversité Paris-Saclay · FRWellcome/Cancer Research UK Gurdon Institute · GB

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748Wellcome Trust 100140
6 · The paper itself

Abstract

TET proteins convert 5-methylcytosine to 5-hydroxymethylcytosine, an emerging dynamic epigenetic state of DNA that can influence transcription. Evidence has linked TET1 function to epigenetic repression complexes, yet mechanistic information, especially for the TET2 and TET3 proteins, remains limited. Here, we show a direct interaction of TET2 and TET3 with O-GlcNAc transferase (OGT). OGT does not appear to influence hmC activity, rather TET2 and TET3 promote OGT activity. TET2/3-OGT co-localize on chromatin at active promoters enriched for H3K4me3 and reduction of either TET2/3 or OGT activity results in a direct decrease in H3K4me3 and concomitant decreased transcription. Further, we show that Host Cell Factor 1 (HCF1), a component of the H3K4 methyltransferase SET1/COMPASS complex, is a specific GlcNAcylation target of TET2/3-OGT, and modification of HCF1 is important for the integrity of SET1/COMPASS. Additionally, we find both TET proteins and OGT activity promote binding of the SET1/COMPASS H3K4 methyltransferase, SETD1A, to chromatin. Finally, studies in Tet2 knockout mouse bone marrow tissue extend and support the data as decreases are observed of global GlcNAcylation and also of H3K4me3, notably at several key regulators of haematopoiesis. Together, our results unveil a step-wise model, involving TET-OGT interactions, promotion of GlcNAcylation, and influence on H3K4me3 via SET1/COMPASS, highlighting a novel means by which TETs may induce transcriptional activation.

Indexed as

DNA MethylationGene Expression RegulationTranscription, Genetic5-MethylcytosineAmino Acid SequenceAnimalsBlotting, WesternCell ProliferationCells, CulturedChromatin ImmunoprecipitationCpG IslandsCytosineDioxygenasesDNA-Binding ProteinsEpigenesis, GeneticGlycosylation5-hydroxymethylcytosine5-MethylcytosineCytosineDioxygenasesDNA-Binding ProteinsHCFC1 protein, humanHistone-Lysine N-MethyltransferaseHistonesHost Cell Factor C1N-AcetylglucosaminyltransferasesO-GlcNAc transferaseProto-Oncogene ProteinsSetd1A protein, humanTET2 protein, humanTET3 protein, human

Identifiers

PMID23353889
PMCPMC3590984
OpenAlexW2107279676

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.