Non-classical genomic estrogen receptor (ER)/specificity protein and ER/activating protein-1 signaling pathways

Safe, Stephen; Kim, Kyoungkim

doi:10.1677/jme-08-0103

Cited by 368Estrogen and related hormone effectsGenomics and Chromatin DynamicsEpigenetics and DNA Methylation

Non-classical genomic estrogen receptor (ER)/specificity protein and ER/activating protein-1 signaling pathways

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Safe, Stephen, Kim, Kyoungkim·2008·Journal of Molecular Endocrinology

DOI 10.1677/jme-08-0103PMC PMC2582054

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Abstract

17β-Estradiol binds to the estrogen receptor (ER) to activate gene expression or repression and this involves both genomic (nuclear) and non-genomic (extranuclear) pathways. Genomic pathways include the classical interactions of ligand-bound ER dimers with estrogen-responsive elements in target gene promoters. ER-dependent activation of gene expression also involves DNA-bound ER that subsequently interacts with other DNA-bound transcriptions factors and direct ER-transcription factor (protein–protein) interactions where ER does not bind promoter DNA. Ligand-induced activation of ER/specificity protein (Sp) and ER/activating protein-1 [(AP-1); consisting of jun/fos] complexes are important pathways for modulating expression of a large number of genes. This review summarizes some of the characteristics of ER/Sp- and ER/AP-1-mediated transactivation, which are dependent on ligand structure, cell context, ER-subtype (ERα and ERβ), and Sp protein (SP1, SP3, and SP4) and demonstrates that this non-classical genomic pathway is also functional in vivo .

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Classical genomic ER action typically occurs within hours, leading to activation or repression of target genes; ligand-activated ER binds as a dimer directly to an estrogen response element in target gene promoters.
“The classical genomic action mechanism of ER action typically occurs within hours, leading to activation or repression of target genes.”
From Estrogen deficiency and the origin of obesity during menopause (2014) · cites this paper as [52]

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Authors: Safe, S., & Kim, K.
Affiliations: Texas A&M University (US)
Texas A&M Health Science Center (US)
ORCID: Safe, Stephen
Venue: Journal of Molecular Endocrinology
Publisher: Bioscientifica
Published: 2008-09-04
Volume: 41
Issue: 5
Pages: 263-275
ISSN: 0952-5041 (ISSN-L)
1479-6813
DOI: 10.1677/jme-08-0103
PMC: PMC2582054
OpenAlex: W2142895048
Cited by: 368
References: 136
Citations by year: 2026: 5 · 2025: 13 · 2024: 11 · 2023: 13 · 2022: 33 · 2021: 22 · 2020: 16 · 2019: 15 · 2018: 18 · 2017: 15 · 2016: 22 · 2015: 20 · 2014: 19 · 2013: 29 · 2012: 20
FWCI: 3.00
Type: journal article
Language: en
Update notices: correction (2009-04-01)
Open access: bronze
doi.org
Locations: Journal of Molecular Endocrinology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Environmental Health Sciences (ES 04917, P42ES004917)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords: estrogen receptor, non-genomic estrogen signaling, specificity proteins, activator protein-1, estrogen response element, estrogen receptor alpha, estrogen receptor beta, ligand structure, transcription factor interaction, estradiol
MeSH terms: Animals, Estradiol, Gene Expression Regulation, Humans, Ligands, Receptors, Estrogen, Signal Transduction, Sp1 Transcription Factor, Transcription Factor AP-1, Cell Line, Tumor

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Non-classical genomic estrogen receptor (ER)/specificity protein and ER/activating protein-1 signaling pathways

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