Evidence map›Paper›PMID 23821662›Full record

ArticleNucleic acids research2013

Estrogen represses gene expression through reconfiguring chromatin structures.

Hatice Ulku Osmanbeyoglu, Kevin N Lu, Steffi Oesterreich, Roger S Day, Panayiotis V Benos, Claudia Coronnello, Xinghua Lu

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Neonatal diethylstilbestrol exposure disrupts uterine epithelial apical-basal polarity and partial EMT state.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Estrogens and stem cells in thyroid cancer.Frontiers in endocrinology · 2014
    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

7 authors at 1 institution in 1 country.

Hatice Ulku OsmanbeyogluDepartment of Biomedical Informatics, University of Pittsburgh, Pittsburgh, PA, USA, Department of Computer Science, University of Pittsburgh, Pittsburgh, PA, USA, Department of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA, Women's Cancer Research Center, University of Pittsburgh, Pittsburgh, PA, USA, Department of Computational and Systems Biology, University of Pittsburgh, Pittsburgh, PA, USA and Fondazione Ri.MED, Palermo, Italy.
Kevin N Lu
Steffi Oesterreich
Roger S Day
Panayiotis V Benos
Claudia Coronnello
Xinghua Lu
University of Pittsburgh · US

Funding

Statistical methods for integromics discoveriesR01LM010144 · NLM · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LU, XINGHUA · 2009 to 2013
$1.6M
Ontology-Driven Methods for Knowledge Acquisition and Knowledge DiscoveryR01LM011155 · NLM · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LU, XINGHUA · 2011 to 2014
$1.2M
NLM NIH HHS R01 LM010144NLM NIH HHS R01 LM011155
6 · The paper itself

Abstract

Estrogen regulates over a thousand genes, with an equal number of them being induced or repressed. The distinct mechanisms underlying these dual transcriptional effects remain largely unknown. We derived comprehensive views of the transcription machineries assembled at estrogen-responsive genes through integrating multiple types of genomic data. In the absence of estrogen, the majority of genes formed higher-order chromatin structures, including DNA loops tethered to protein complexes involving RNA polymerase II (Pol II), estrogen receptor alpha (ERα) and ERα-pioneer factors. Genes to be 'repressed' by estrogen showed active transcription at promoters and throughout the gene bodies; genes to be 'induced' exhibited active transcription initiation at promoters, but with transcription paused in gene bodies. In the presence of estrogen, the majority of estrogen-induced genes retained the original higher-order chromatin structures, whereas most estrogen-repressed genes underwent a chromatin reconfiguration. For estrogen-induced genes, estrogen enhances transcription elongation, potentially through recruitment of co-activators or release of co-repressors with unique roles in elongation. For estrogen-repressed genes, estrogen treatment leads to chromatin structure reconfiguration, thereby disrupting the originally transcription-efficient chromatin structures. Our in silico studies have shown that estrogen regulates gene expression, at least in part, through modifying previously assembled higher-order complexes, rather than by facilitating de novo assembly of machineries.

Indexed as

Gene Expression RegulationTranscription, GeneticChromatinComputer SimulationEstrogen Receptor alphaEstrogensHistonesHumansMCF-7 CellsPromoter Regions, GeneticRNA Polymerase IITranscription FactorsChromatinEstrogen Receptor alphaEstrogensHistonesRNA Polymerase IITranscription Factors

Identifiers

PMID23821662
PMCPMC3783169
OpenAlexW1980128547

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.