Evidence map›Paper›PMID 22071320›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2012

Aryl hydrocarbon receptor modulation of estrogen receptor α-mediated gene regulation by a multimeric chromatin complex involving the two receptors and the coregulator RIP140.

Zeynep Madak-Erdogan, Benita S Katzenellenbogen

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Functional genomic analysis of non-canonical DNA regulatory elements of the aryl hydrocarbon receptor.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. RIP140 regulatesCancer drug resistance (Alhambra, Calif.) · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Zeynep Madak-ErdoganDepartment of Molecular and Integrative Physiology, University of Illinois, Urbana, Illinois 61801, USA.
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
Pharmacokinetics, Bioavailability, and Metabolism/Daniel R. DoergeP50AT006268 · NCCIH · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI HELFERICH, WILLIAM G · 2010 to 2015
$7.6M
NCCIH NIH HHS P50 AT006268NIEHS NIH HHS T32ES007326
6 · The paper itself

Abstract

Although crosstalk between aryl hydrocarbon receptor (AhR) and estrogen receptor α (ERα) is well established, the mechanistic basis and involvement of other proteins in this process are not known. Because we observed an enrichment of AhR-binding motifs in ERα-binding sites of many estradiol (E2)-regulated genes, we investigated how AhR might modulate ERα-mediated gene transcription in breast cancer cells. Gene regulations were categorized based on their pattern of stimulation by E2 and/or dioxin and were denoted E2-responsive, dioxin-responsive, or responsive to either ligand. ERα, AhR, aryl hydrocarbon receptor translocator, and receptor interacting protein 140 (RIP140) were recruited to gene regulatory regions in a gene-specific and E2/dioxin ligand-specific manner. Knockdown of AhR markedly increased the expression of ERα-mediated genes upon E2 treatment. This was not attributable to a change in ERα level, or recruitment of ERα, phosphoSer5-RNA Pol II, or several coregulators but rather was associated with greatly diminished recruitment of the coregulator RIP140 to gene regulatory sites. Changing the cellular level of RIP140 revealed coactivator or corepressor roles for this coregulator in E2- and dioxin-mediated gene regulation, the choice of which was determined by the presence or absence of ERα at gene regulatory sites. Coimmunoprecipitation and chromatin immunoprecipitation (ChIP)-reChIP studies documented that E2- or dioxin-promoted formation of a multimeric complex of ERα, AhR, and RIP140 at ERα-binding sites of genes regulated by either E2 or dioxin. Our findings highlight the importance of cross-regulation between AhR and ERα and a novel mechanism by which AhR controls, through modulating the recruitment of RIP140 to ERα-binding sites, the kinetics and magnitude of ERα-mediated gene stimulation.

Indexed as

Chromatin Assembly and DisassemblyGene Expression Regulation, NeoplasticReceptor Cross-TalkAdaptor Proteins, Signal TransducingBasic Helix-Loop-Helix ProteinsBinding SitesBreast NeoplasmsCell Line, TumorChromatin ImmunoprecipitationDioxinsEstradiolEstrogen Receptor alphaFemaleHumansKineticsNuclear ProteinsAdaptor Proteins, Signal TransducingAHR protein, humanBasic Helix-Loop-Helix ProteinsDioxinsESR1 protein, humanEstradiolEstrogen Receptor alphaNRIP1 protein, humanNuclear ProteinsNuclear Receptor Interacting Protein 1Receptors, Aryl HydrocarbonRNA, MessengerRNA Polymerase II

Identifiers

PMID22071320
PMCPMC3262852
OpenAlexW2120712472

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.