ArticleThe EMBO journal2004
Transcriptional complexes engaged by apo-estrogen receptor-alpha isoforms have divergent outcomes.
Article in The EMBO journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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.
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.
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Who cites it
49 citing papers in PubMed, 101 citations in OpenAlex.
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- Targeting estrogen receptor alpha in breast cancer for novel therapies resistance mechanisms and future directions.Discover oncology · 2025Review
- Genomic Crosstalk Between Nuclear Receptors in Hormone-dependent Cancers.Endocrinology · 2025Review
- Correlation between the RNA Expression and the DNA Methylation of Estrogen Receptor Genes in Normal and Malignant Human Tissues.Current issues in molecular biology · 2024Article
- Sex-Specific Regulation of β-Secretase: A Novel Estrogen Response Element (ERE)-Dependent Mechanism in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Mapping Isoform Abundance and Interactome of the Endogenous TMPRSS2-ERG Fusion Protein by Orthogonal Immunoprecipitation-Mass Spectrometry Assays.Molecular & cellular proteomics : MCP · 2021Article
- Matters of life and death: How estrogen and estrogen receptor binding to the immunoglobulin heavy chain locus may influence outcomes of infection, allergy, and autoimmune disease.Cellular immunology · 2019Review
- Molecular mechanism of estrogen-estrogen receptor signaling.Reproductive medicine and biology · 2017Review
- The AF-1-deficient estrogen receptor ERα46 isoform is frequently expressed in human breast tumors.Breast cancer research : BCR · 2016Article
- Early-late genes of the ecdysone cascade as models for transcriptional studies.Cell cycle (Georgetown, Tex.) · 2015Article
- ARID3B expression in primary breast cancers and breast cancer-derived cell lines.Cellular oncology (Dordrecht, Netherlands) · 2014Article
- Endocrine disruptors fludioxonil and fenhexamid stimulate miR-21 expression in breast cancer cells.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- Estrogen-induced upregulation and 3'-UTR shortening of CDC6.Nucleic acids research · 2012Article
- Chromatin immunoprecipitation assay as a tool for analyzing transcription factor activity.Methods in molecular biology (Clifton, N.J.) · 2012Article
- A self-organized model for cell-differentiation based on variations of molecular decay rates.PloS one · 2012Article
- Histone deacetylase 1 (HDAC1) participates in the down-regulation of corticotropin releasing hormone gene (crh) expression.Physiology & behavior · 2011Article
- Estrogen receptors similarly mediate the effects of 17β-estradiol on cellular responses but differ in their potencies.Endocrine · 2011Article
- Estrogen receptor alpha 46 is reduced in tamoxifen resistant breast cancer cells and re-expression inhibits cell proliferation and estrogen receptor alpha 66-regulated target gene transcription.Molecular and cellular endocrinology · 2010Article
- Identification of a hormone-regulated dynamic nuclear actin network associated with estrogen receptor alpha in human breast cancer cell nuclei.Molecular & cellular proteomics : MCP · 2010Article
- Cooperative activation of cyclin D1 and progesterone receptor gene expression by the SRC-3 coactivator and SMRT corepressor.Molecular endocrinology (Baltimore, Md.) · 2010Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Unliganded (apo-) estrogen receptor alpha (ERalpha, NR3A1) is classically considered as transcriptionally unproductive. Reassessing this paradigm demonstrated that apo-human ERalpha (ERalpha66) and its N-terminally truncated isoform (ERalpha46) are both predominantly nuclear transcription factors that cycle on the endogenous estrogen-responsive pS2 gene promoter in vivo. Importantly, isoform-specific consequences occur in terms of poising the promoter for transcription, as evaluated by determining (i) the engagement of several cofactors and the resulting nucleosomal organization; and (ii) the CpG methylation state of the pS2 promoter. Although transcriptionally unproductive, cycling of apo-ERalpha66 prepares the promoter to respond to ligand, through sequentially targeting chromatin remodeling complexes and general transcription factors. Additionally, apo-ERalpha46 recruits corepressors, following engagement of cofactors identical to those recruited by apo-ERalpha66. Together, these data describe differential activities of ERalpha isoforms. Furthermore, they depict the maintenance of a promoter in a repressed state as a cyclical process that is intrinsically dependent on initial poising of the promoter.
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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.