Evidence map›Paper›PMID 23882126›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013

Mechanisms enforcing the estrogen receptor β selectivity of botanical estrogens.

Yan Jiang, Ping Gong, Zeynep Madak-Erdogan, Teresa Martin, Muthu Jeyakumar, Kathryn Carlson, Ikhlas Khan, Troy J Smillie, Amar G Chittiboyina, Sateesh C K Rotte and 3 more

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 2 pooled it
4.5field-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

68 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.

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  17. MKK4 Inhibitors-Recent Development Status and Therapeutic Potential.International journal of molecular sciences · 2023
    Review
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8 more citing papers are in PubMed but not listed here.

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

13 authors at 2 institutions in 1 country.

Yan Jiang1Department of Molecular and Integrative Physiology, University of Illinois and College of Medicine at Urbana-Champaign, Urbana, IL 61801, USA. katzenel@illinois.edu.
Ping Gong
Zeynep Madak-Erdogan
Teresa Martin
Muthu Jeyakumar
Kathryn Carlson
Ikhlas Khan
Troy J Smillie
Amar G Chittiboyina
Sateesh C K Rotte
William G Helferich
John A Katzenellenbogen
Benita S Katzenellenbogen
University of Illinois Urbana-Champaign · USUniversity of Mississippi · 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 AT006268NCCIH NIH HHS P50AT006268NIEHS NIH HHS T32 ES007326NIEHS NIH HHS T32ES007326
6 · The paper itself

Abstract

Because little is known about the actions of botanical estrogens (BEs), widely consumed by menopausal women, we investigated the mechanistic and cellular activities of some major BEs. We examined the interactions of genistein, daidzein, equol, and liquiritigenin with estrogen receptors ERα and ERβ, with key coregulators (SRC3 and RIP140) and chromatin binding sites, and the regulation of gene expression and proliferation in MCF-7 breast cancer cells containing ERα and/or ERβ. Unlike the endogenous estrogen, estradiol (E2), BEs preferentially bind to ERβ, but their ERβ-potency selectivity in gene stimulation (340- to 830-fold vs. E2) is enhanced at several levels (coregulator recruitment, chromatin binding); nevertheless, at high (0.1 or 1 μM) concentrations, BEs also fully activate ERα. Because ERα drives breast cancer cell proliferation and ERβ dampens this, the relative levels of these two ERs in target cells and the BE dose greatly affect gene expression and proliferative response and will be crucial determinants of the potential benefits vs. risks of BEs. Our findings reveal key and novel mechanistic differences in the estrogenic activities of BEs vs. E2, with BEs displaying patterns of activity distinctly different from those seen with E2 and provide valuable information to inform future studies.

Indexed as

Adaptor Proteins, Signal TransducingBinding SitesCell ProliferationChromatinDose-Response Relationship, DrugEstradiolEstrogen Receptor alphaEstrogen Receptor betaHumansMCF-7 CellsNuclear ProteinsNuclear Receptor Coactivator 3Nuclear Receptor Interacting Protein 1PhytoestrogensTranscription, GeneticAdaptor Proteins, Signal TransducingChromatinEstradiolEstrogen Receptor alphaEstrogen Receptor betaNCOA3 protein, humanNRIP1 protein, humanNuclear ProteinsNuclear Receptor Coactivator 3Nuclear Receptor Interacting Protein 1Phytoestrogensbreast cancer cellschromatin bindinggene regulationproliferation

Identifiers

PMID23882126
PMCPMC3804744
OpenAlexW2157252247

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.