Evidence map›Paper›PMID 12660164›Full record

ArticleThe EMBO journal2003

Thyroid hormone-regulated enhancer blocking: cooperation of CTCF and thyroid hormone receptor.

Marcus Lutz, Les J Burke, Pascal LeFevre, Fiona A Myers, Alan W Thorne, Colyn Crane-Robinson, Constanze Bonifer, Galina N Filippova, Victor Lobanenkov, Rainer Renkawitz

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
5.1field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Genome-wide analysis of thyroid hormone receptors shared and specific functions in neural cells.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  12. CTCF: the protein, the binding partners, the binding sites and their chromatin loops.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2013
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Does CTCF mediate between nuclear organization and gene expression?BioEssays : news and reviews in molecular, cellular and developmental biology · 2010
    Review
  20. 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

10 authors at 1 institution in 1 country.

Marcus LutzInstitute for Genetics, Justus-Liebig-Universitaet Giessen, Heinrich-Buff-Ring 58-62, D-35392 Giessen, Germany.
Les J Burke
Pascal LeFevre
Fiona A Myers
Alan W Thorne
Colyn Crane-Robinson
Constanze Bonifer
Galina N Filippova
Victor Lobanenkov
Rainer Renkawitz
Goethe University Frankfurt · DE

Funding

Normal and Pathologic Functions of CTCF and Its Distinct Classes of DNA-targetsZIAAI000860 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LOBANENKOV, VICTOR · 2009 to 2025
$15.4M
Transcriptional Regulation Of Ctcf And Boris ExpressionZ01AI000860 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI LOBANENKOV, VICTOR · 2000 to 2008
$1.5M
ROLE OF TRANSCRIPTION FACTOR CTCF IN TUMOR DEVELOPMENTZ01AI000859 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI LOBANENKOV, VICTOR · 2000 to 2003
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6 · The paper itself

Abstract

The highly conserved, ubiquitously expressed, zinc finger protein CTCF is involved in enhancer blocking, a mechanism crucial for shielding genes from illegitimate enhancer effects. Interestingly, CTCF-binding sites are often flanked by thyroid hormone response elements (TREs), as at the chicken lysozyme upstream silencer. Here we identify a similar composite site positioned upstream of the human c-myc gene. For both elements, we demonstrate that thyroid hormone abrogates enhancer blocking. Relief of enhancer blocking occurs even though CTCF remains bound to the lysozyme chromatin. Furthermore, chromatin immunoprecipitation analysis of the lysozyme upstream region revealed that histone H4 is acetylated at the CTCF-binding site. Loss of enhancer blocking by the addition of T3 led to increased histone acetylation, not only at the CTCF site, but also at the enhancer and the promoter. Thus, when TREs are adjacent to CTCF-binding sites, thyroid hormone can regulate enhancer blocking, thereby providing a new property for what was previously thought to be constitutive enhancer shielding by CTCF.

Indexed as

Enhancer Elements, GeneticRepressor ProteinsAcetylationAnimalsBase SequenceCCCTC-Binding FactorChickensDNA-Binding ProteinsElectrophoretic Mobility Shift AssayHistonesHumansK562 CellsMolecular Sequence DataReceptors, Thyroid HormoneSequence Homology, Nucleic AcidThyroid HormonesCCCTC-Binding FactorCTCF protein, humanDNA-Binding ProteinsHistonesReceptors, Thyroid HormoneRepressor ProteinsThyroid HormonesTranscription Factors

Identifiers

PMID12660164
PMCPMC152892
OpenAlexW2088661602

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.