Evidence map›Paper›PMID 21451524›Full record

ArticleNature2011

Dual functions of Tet1 in transcriptional regulation in mouse embryonic stem cells.

Hao Wu, Ana C D'Alessio, Shinsuke Ito, Kai Xia, Zhibin Wang, Kairong Cui, Keji Zhao, Yi Eve Sun, Yi Zhang

Open access · greenAbstract read
In one paragraph

Article in Nature, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 400 papers.

0numbers the graph read from it
0cells of the map it votes in
400citing papers in PubMed
34.3field-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

400 citing papers in PubMed, 642 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  10. Review
  11. Mechanisms of human germ cell development.Nature reviews. Molecular cell biology · 2026
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

340 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Hao WuDepartment of Molecular & Medical Pharmacology, UCLA David Geffen School of Medicine, Los Angeles, California 90095, USA.
Ana C D'Alessio
Shinsuke Ito
Kai Xia
Zhibin Wang
Kairong Cui
Keji Zhao
Yi Eve Sun
Yi Zhang
Howard Hughes Medical Institute · USNational Institutes of Health · USUniversity of North Carolina at Chapel Hill · USJohns Hopkins University · USUniversity of California, Los Angeles · US

Funding

Genome-wide mapping of histone modificationsZIAHL005801 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ZHAO, KEJI · 2009 to 2025
$24.0M
Epigenetic Regulation of Hematopoietic Stem CellsZIAHL006031 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ZHAO, KEJI · 2009 to 2025
$16.6M
Mechanisms of Polycomb SilencingR01GM068804 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, YI · 2003 to 2010
$2.1M
Function of MeCP2 in hESC-derived neuronsR56MH082068 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SUN, YI EVE · 2008 to 2008
$339k
Howard Hughes Medical InstituteIntramural NIH HHSNIGMS NIH HHS GM68804NIGMS NIH HHS R01 GM068804NIMH NIH HHS R56 MH082068NIMH NIH HHS R56MH082068
6 · The paper itself

Abstract

Epigenetic modification of the mammalian genome by DNA methylation (5-methylcytosine) has a profound impact on chromatin structure, gene expression and maintenance of cellular identity. The recent demonstration that members of the Ten-eleven translocation (Tet) family of proteins can convert 5-methylcytosine to 5-hydroxymethylcytosine raised the possibility that Tet proteins are capable of establishing a distinct epigenetic state. We have recently demonstrated that Tet1 is specifically expressed in murine embryonic stem (ES) cells and is required for ES cell maintenance. Using chromatin immunoprecipitation coupled with high-throughput DNA sequencing, here we show in mouse ES cells that Tet1 is preferentially bound to CpG-rich sequences at promoters of both transcriptionally active and Polycomb-repressed genes. Despite an increase in levels of DNA methylation at many Tet1-binding sites, Tet1 depletion does not lead to downregulation of all the Tet1 targets. Interestingly, although Tet1-mediated promoter hypomethylation is required for maintaining the expression of a group of transcriptionally active genes, it is also involved in repression of Polycomb-targeted developmental regulators. Tet1 contributes to silencing of this group of genes by facilitating recruitment of PRC2 to CpG-rich gene promoters. Thus, our study not only establishes a role for Tet1 in modulating DNA methylation levels at CpG-rich promoters, but also reveals a dual function of Tet1 in promoting transcription of pluripotency factors as well as participating in the repression of Polycomb-targeted developmental regulators.

Indexed as

DNA MethylationGene SilencingTranscription, Genetic5-MethylcytosineAnimalsCell LineChromatinCpG IslandsCytosineDNA-Binding ProteinsEmbryonic Stem CellsGene Expression Regulation, DevelopmentalGenomeMicePolycomb-Group ProteinsPromoter Regions, Genetic5-hydroxymethylcytosine5-MethylcytosineChromatinCytosineDNA-Binding ProteinsPolycomb-Group ProteinsProto-Oncogene ProteinsRepressor ProteinsTET1 protein, mouse

Identifiers

PMID21451524
PMCPMC3539771
OpenAlexW2077359452

What OpenQuestion holds

Textmetadata
LicenceTDM
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.