ArticleProceedings of the National Academy of Sciences of the United States of America1999
Estradiol repression of tumor necrosis factor-alpha transcription requires estrogen receptor activation function-2 and is enhanced by coactivators.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 199 citations in OpenAlex.
- Incidence and influencing factors of occupational pneumoconiosis: a systematic review and meta-analysis.BMJ open · 2023Pooled it
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- Sex Steroid Hormone Regulation of T-Cell Function and Antitumor Immunity.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Review
- Th2 cytokine-induced mucociliary remodeling in chronic rhinosinusitis: implications for antiviral defense and epithelial function.Respiratory research · 2026Article
- Estrogen receptor 1 activation suppresses microglia-derived Tnf-α signaling as a photoreceptor self-protection mechanism.Journal of neuroinflammation · 2025Article
- Deletion of the X-chromosomal geneScience translational medicine · 2025Article
- Article
- Cystatin M/E ameliorates bone resorption through increasing osteoclastic cell estrogen influx.Research square · 2024Article
- Biological differences underlying sex and gender disparities in bladder cancer: current synopsis and future directions.Oncogenesis · 2023Review
- Assessment of gender differences in some inflammatory cytokines of tuberculosis patients before and during treatment.African health sciences · 2023Article
- Sex hormone influence on female-biased autoimmune diseases hints at puberty as an important factor in pathogenesis.Frontiers in pediatrics · 2023Review
- Steroid nuclear receptor coactivator 2 controls immune tolerance by promoting induced TScience advances · 2022Article
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- Human Immunodeficiency Virus Is Associated With Higher Levels of Systemic Inflammation Among Kenyan Adults Despite Viral Suppression.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2021Article
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- Depression symptoms mediate the association between workplace stress and interleukin 6 in women, but not men: The Whitehall II study.Brain, behavior, & immunity - health · 2021Article
- Differential activation of Gsk-3β in the cortex and the hippocampus induces cognitive and behavioural impairments in middle-aged ovariectomized rat.Comprehensive psychoneuroendocrinology · 2020Article
- Possible protective role of 17β-estradiol against COVID-19.Journal of allergy and infectious diseases · 2020Article
- Estrogen receptor alpha differentially modulates host immunity in the bladder and kidney in response to urinary tract infection.American journal of clinical and experimental urology · 2019Article
- Estriol Reduces Pulmonary Immune Cell Recruitment and Inflammation to Protect Female Mice From Severe Influenza.Endocrinology · 2018Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The tumor necrosis factor-alpha (TNF-alpha) promoter was used to explore the molecular mechanisms of estradiol (E(2))-dependent repression of gene transcription. E(2) inhibited basal activity and abolished TNF-alpha activation of the TNF-alpha promoter. The E(2)-inhibitory element was mapped to the -125 to -82 region of the TNF-alpha promoter, known as the TNF-responsive element (TNF-RE). An AP-1-like site in the TNF-RE is essential for repression activity. Estrogen receptor (ER) beta is more potent than ERalpha at repressing the -1044 TNF-alpha promoter and the TNF-RE upstream of the herpes simplex virus thymidine kinase promoter, but weaker at activating transcription through an estrogen response element. The activation function-2 (AF-2) surface in the ligand-binding domain is required for repression, because anti-estrogens and AF-2 mutations impair repression. The requirement of the AF-2 surface for repression is probably due to its capacity to recruit p160 coactivators or related coregulators, because overexpressing the coactivator glucocorticoid receptor interacting protein-1 enhances repression, whereas a glucocorticoid receptor interacting protein-1 mutant unable to interact with the AF-2 surface is ineffective. Furthermore, receptor interacting protein 140 prevents repression by ERbeta, probably by interacting with the AF-2 surface and blocking the binding of endogenous coactivators. These studies demonstrate that E(2)-mediated repression requires the AF-2 surface and the participation of coactivators or other coregulatory proteins.
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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.