Evidence map›Paper›PMID 19188451›Full record

ArticleMolecular and cellular biology2009

Estrogen receptor alpha represses transcription of early target genes via p300 and CtBP1.

Fabio Stossi, Zeynep Madak-Erdogan, Benita S Katzenellenbogen

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 66 citations in OpenAlex.

  1. 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
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  6. Coregulators Reside withinInternational journal of molecular sciences · 2023
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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

3 authors at 1 institution in 1 country.

Fabio StossiDepartment of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801-3704, USA.
Zeynep Madak-Erdogan
Benita S Katzenellenbogen
University of Illinois Urbana-Champaign · US

Funding

Research Training Program in Toxicology and Environmental HealthT32ES007326 · NIEHS · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI Jodi A. Flaws · 2000 to 2026
$8.7M
ANTIESTROGENS: MECHANISM OF ANTAGONIST ACTIONR01CA018119 · NCI · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KATZENELLENBOGEN, BENITA S · 1985 to 2008
$2.8M
ANTIESTROGENS: MECHANISM OF ANTAGONIST ACTIONR37CA018119 · NCI · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI KATZENELLENBOGEN, BENITA S · 1991 to 1998
–
NCI NIH HHS CA18119NCI NIH HHS R01 CA018119NIEHS NIH HHS T32 ES007326NIEHS NIH HHS T32 ES07326
6 · The paper itself

Abstract

The regulation of gene expression by nuclear receptors controls the phenotypic properties and diverse biologies of target cells. In breast cancer cells, estrogen receptor alpha (ERalpha) is a master regulator of transcriptional stimulation and repression, yet the mechanisms by which agonist-bound ERalpha elicits repression are poorly understood. We analyzed early estrogen-repressed genes and found that ERalpha is recruited to ERalpha binding sites of these genes, albeit more transiently and less efficiently than for estrogen-stimulated genes. Of multiple cofactors studied, only p300 was recruited to ERalpha binding sites of repressed genes, and its knockdown prevented estrogen-mediated gene repression. Because p300 is involved in transcription initiation, we tested whether ERalpha might be trying to stimulate transcription at repressed genes, with ultimately failure and a shift to a repressive program. We found that estrogen increases transcription in a rapid but transient manner at early estrogen-repressed genes but that this is followed by recruitment of the corepressor CtBP1, a p300-interacting partner that plays an essential role in the repressive process. Thus, at early estrogen-repressed genes, ERalpha initiates transient stimulation of transcription but fails to maintain the transcriptional process observed at estrogen-stimulated genes; rather, it uses p300 to recruit CtBP1-containing complexes, eliciting chromatin modifications that lead to transcriptional repression.

Indexed as

Transcription, GeneticAcetylationAlcohol OxidoreductasesBinding SitesCell Line, TumorDNA-Binding ProteinsE1A-Associated p300 ProteinEstradiolEstrogen Receptor alphaGene Expression Regulation, NeoplasticHistonesHumansLysineModels, GeneticProtein BindingProtein TransportAlcohol OxidoreductasesC-terminal binding proteinDNA-Binding ProteinsE1A-Associated p300 ProteinEP300 protein, humanESR1 protein, humanEstradiolEstrogen Receptor alphaHistonesLysineRepressor ProteinsRNA, Small Interfering

Identifiers

PMID19188451
PMCPMC2655624
OpenAlexW2129737216

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.