Evidence map›Paper›PMID 25294833›Full record

ArticleNucleic acids research2014

CTCF induces histone variant incorporation, erases the H3K27me3 histone mark and opens chromatin.

Oliver Weth, Christine Paprotka, Katharina Günther, Astrid Schulte, Manuel Baierl, Joerg Leers, Niels Galjart, Rainer Renkawitz

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Benefiting from the intrinsic role of epigenetics to predict patterns of CTCF binding.Computational and structural biotechnology journal · 2023
    Article
  12. Review
  13. Zinc finger protein 280C contributes to colorectal tumorigenesis by maintaining epigenetic repression at H3K27me3-marked loci.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  14. Article
  15. Deciphering the genetic code of DNA methylation.Briefings in bioinformatics · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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.

Oliver WethInstitute for Genetics, Justus-Liebig-University, 35392 Giessen, Germany.
Christine PaprotkaInstitute for Genetics, Justus-Liebig-University, 35392 Giessen, Germany.
Katharina GüntherInstitute for Genetics, Justus-Liebig-University, 35392 Giessen, Germany.
Astrid SchulteInstitute for Genetics, Justus-Liebig-University, 35392 Giessen, Germany.
Manuel BaierlInstitute for Genetics, Justus-Liebig-University, 35392 Giessen, Germany.
Joerg LeersInstitute for Genetics, Justus-Liebig-University, 35392 Giessen, Germany.
Niels GaljartDepartment of Cell Biology and Genetics, Erasmus MC, 3000 CA Rotterdam, The Netherlands.
Rainer RenkawitzInstitute for Genetics, Justus-Liebig-University, 35392 Giessen, Germany Rainer.Renkawitz@gen.bio.uni-giessen.de.ORCID http://orcid.org/0000-0002-2591-1332
Justus-Liebig-Universität Gießen · DEErasmus MC · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulators functionally separate active chromatin domains from inactive ones. The insulator factor, CTCF, has been found to bind to boundaries and to mediate insulator function. CTCF binding sites are depleted for the histone modification H3K27me3 and are enriched for the histone variant H3.3. In order to determine whether demethylation of H3K27me3 and H3.3 incorporation are a requirement for CTCF binding at domain boundaries or whether CTCF causes these changes, we made use of the LacI DNA binding domain to control CTCF binding by the Lac inducer IPTG. Here we show that, in contrast to the related factor CTCFL, the N-terminus plus zinc finger domain of CTCF is sufficient to open compact chromatin rapidly. This is preceded by incorporation of the histone variant H3.3, which thereby removes the H3K27me3 mark. This demonstrates the causal role for CTCF in generating the chromatin features found at insulators. Thereby, spreading of a histone modification from one domain through the insulator into the neighbouring domain is inhibited.

Indexed as

Insulator ElementsCCCTC-Binding FactorCell LineChromatinDNA-Binding ProteinsHeLa CellsHistonesHumansMethylationRepressor ProteinsZinc FingersCCCTC-Binding FactorChromatinCTCFL protein, humanCTCF protein, humanDNA-Binding ProteinsHistonesRepressor Proteins

Identifiers

PMID25294833
PMCPMC4231773
OpenAlexW2060800766

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.