ArticleThe Journal of biological chemistry2009
Genomic responses from the estrogen-responsive element-dependent signaling pathway mediated by estrogen receptor alpha are required to elicit cellular alterations.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Pre-Treatment with Estradiol, But not Progesterone, Exacerbates DSS Colitis: Dysregulated Innate Immunity and Impaired Epithelial Damage Response.Inflammation · 2026Article
- Yippee-like protein Moh1 links gene expression to metabolism and selective stress resistance inMicrobial cell (Graz, Austria) · 2026Article
- CXXC5 is a ubiquitinated protein and is degraded by the ubiquitin-proteasome pathway.Protein science : a publication of the Protein Society · 2025Article
- Estrogenic endocrine disruptor exposure directly impacts erectile function.Communications biology · 2024Article
- Dynamic proximity interaction profiling suggests that YPEL2 is involved in cellular stress surveillance.Protein science : a publication of the Protein Society · 2024Article
- Increased FOXA1 levels induce apoptosis and inhibit proliferation in FOXA1-low expressing basal breast cancer cells.American journal of cancer research · 2022Article
- A prelude to the proximity interaction mapping of CXXC5.Scientific reports · 2021Article
- A CpG island promoter drives the CXXC5 gene expression.Scientific reports · 2021Article
- Effects of Estradiol on Immunoglobulin G Glycosylation: Mapping of the Downstream Signaling Mechanism.Frontiers in immunology · 2021Article
- CXXC5 as an unmethylated CpG dinucleotide binding protein contributes to estrogen-mediated cellular proliferation.Scientific reports · 2020Article
- Molecular mechanism of estrogen-estrogen receptor signaling.Reproductive medicine and biology · 2017Review
- Estradiol-Estrogen Receptor α Mediates the Expression of the CXXC5 Gene through the Estrogen Response Element-Dependent Signaling Pathway.Scientific reports · 2016Article
- Using the canary genome to decipher the evolution of hormone-sensitive gene regulation in seasonal singing birds.Genome biology · 2015Article
- Nuclear Receptor Signaling Atlas: Opening Access to the Biology of Nuclear Receptor Signaling Pathways.PloS one · 2015Article
- Article
- Dynamic estrogen receptor interactomes control estrogen-responsive trefoil Factor (TFF) locus cell-specific activities.Molecular and cellular biology · 2014Article
- The ligand-mediated nuclear mobility and interaction with estrogen-responsive elements of estrogen receptors are subtype specific.Journal of molecular endocrinology · 2012Article
- Estrogen receptors similarly mediate the effects of 17β-estradiol on cellular responses but differ in their potencies.Endocrine · 2011Article
- Designer monotransregulators provide a basis for a transcriptional therapy for de novo endocrine-resistant breast cancer.Molecular medicine (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Estrogen (E2) signaling is conveyed by the transcription factors estrogen receptor (ER) alpha and beta. ERs modulate the expression of genes involved in cellular proliferation, motility, and death. The regulation of transcription by E2-ERalpha through binding to estrogen-responsive elements (EREs) in DNA constitutes the ERE-dependent signaling pathway. E2-ERalpha also modulates gene expression by interacting with transregulators bound to cognate DNA-regulatory elements, and this regulation is referred to as the ERE-independent signaling pathway. The relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. To address this issue, we engineered an ERE-binding defective ERalpha mutant (ERalpha(EBD)) by changing residues in an alpha-helix of the protein involved in DNA binding to render the receptor functional only through the ERE-independent signaling pathway. Using recombinant adenovirus-infected ER-negative MDA-MB-231 cells derived from a breast adenocarcinoma, we found that E2-ERalpha(EBD) modulated the expression of a subset of ERalpha-responsive genes identified by microarrays and verified by quantitative PCR. However, E2-ERalpha(EBD) did not affect cell cycle progression, cellular growth, death, or motility in contrast to E2-ERalpha.ERalpha(EBD) in the presence of E2 was also ineffective in inducing phenotypic alterations in ER-negative U-2OS cells derived from an osteosarcoma. E2-ERalpha, on the other hand, effectively repressed growth in this cell line. Our findings suggest that genomic responses from the ERE-dependent signaling pathway are required for E2-ERalpha to induce alterations in cellular responses.
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Registered trials
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.