Evidence map›Paper›PMID 26397890›Full record

ArticleStem cell research2015

Differential regulation of genomic imprinting by TET proteins in embryonic stem cells.

Lizhi Liu, Shi-Qing Mao, Chelsea Ray, Yu Zhang, Fong T Bell, Sheau-Fang Ng, Guo-Liang Xu, Xiajun Li

Open access · goldAbstract read
In one paragraph

Article in Stem cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. TET3 protects theiScience · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Epigenetic dynamics in cancer stem cell dormancy.Cancer metastasis reviews · 2020
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
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

8 authors at 2 institutions in 2 countries.

Lizhi LiuBlack Family Stem Cell Institute, Department of Developmental and Regenerative Biology, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; Black Family Stem Cell Institute, Department of Oncological Sciences, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Shi-Qing MaoState Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China.
Chelsea RayBlack Family Stem Cell Institute, Department of Developmental and Regenerative Biology, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; Black Family Stem Cell Institute, Department of Oncological Sciences, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Yu ZhangBlack Family Stem Cell Institute, Department of Developmental and Regenerative Biology, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; Black Family Stem Cell Institute, Department of Oncological Sciences, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Fong T BellBlack Family Stem Cell Institute, Department of Developmental and Regenerative Biology, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; Black Family Stem Cell Institute, Department of Oncological Sciences, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Sheau-Fang NgBlack Family Stem Cell Institute, Department of Developmental and Regenerative Biology, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; Black Family Stem Cell Institute, Department of Oncological Sciences, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Guo-Liang XuState Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China.
Xiajun LiBlack Family Stem Cell Institute, Department of Developmental and Regenerative Biology, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA; Black Family Stem Cell Institute, Department of Oncological Sciences, Graduate School of Biological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA. Electronic address: xiajun.li@mssm.edu.
Icahn School of Medicine at Mount Sinai · USChinese Academy of Sciences · CN

Funding

Acquisition and maintenance of DNA methylation in genomic imprintingR01GM093335 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LI, XIAJUN · 2010 to 2014
$1.6M
NIGMS NIH HHS R01 GM093335NIGMS NIH HHS R01GM093335
6 · The paper itself

Abstract

TET proteins have been found to play an important role in active demethylation at CpG sites in mammals. There are some reports implicating their functions in removal of DNA methylation imprint at the imprinted regions in the germline. However, it is not well established whether TET proteins can also be involved in demethylation of DNA methylation imprint in embryonic stem (ES) cells. Here we report that loss of TET proteins caused a significant increase in DNA methylation at the Igf2-H19 imprinted region in ES cells. We also observed a variable increase in DNA methylation at the Peg1 imprinted region in the ES clones devoid of TET proteins, in particular in the differentiated ES cells. By contrast, we did not observe a significant increase of DNA methylation imprint at the Peg3, Snrpn and Dlk1-Dio3 imprinted regions in ES cells lacking TET proteins. Interestingly, loss of TET proteins did not result in a significant increase of DNA methylation imprint at the Igf2-H19 and Peg1 imprinted regions in the embryoid bodies (EB). Therefore, TET proteins seem to be differentially involved in maintaining DNA methylation imprint at a subset of imprinted regions in ES cells and EBs.

Indexed as

Genomic ImprintingAnimalsCalcium-Binding ProteinsCpG IslandsDioxygenasesDNA-Binding ProteinsDNA MethylationEmbryonic Stem CellsInsulin-Like Growth Factor IIIntercellular Signaling Peptides and ProteinsIodide PeroxidaseMiceProteinsProto-Oncogene ProteinsRNA, Long NoncodingsnRNP Core ProteinsCalcium-Binding ProteinsDioxygenasesDlk1 protein, mouseDNA-Binding ProteinsH19 long non-coding RNAInsulin-Like Growth Factor IIIntercellular Signaling Peptides and ProteinsIodide Peroxidaseiodothyronine deiodinase type IIImesoderm specific transcript proteinProteinsProto-Oncogene ProteinsRNA, Long NoncodingsnRNP Core ProteinsTET1 protein, mouseTet2 protein, mouseTet3 protein, mouseBisulfite sequencingCOBRA analysisDNA methylationEBES cellsGenomic imprintingTET

Identifiers

PMID26397890
PMCPMC4618460
OpenAlexW1708000124

What OpenQuestion holds

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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.