ArticleThe Journal of biological chemistry2010
Estrogen inhibits transforming growth factor beta signaling by promoting Smad2/3 degradation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.
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
106 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.
- Exploring associations between estrogen and gene candidates identified by coronary artery disease genome-wide association studies.Frontiers in cardiovascular medicine · 2025Pooled it
- Computational modeling identifies protective mechanisms of estrogen and testosterone against atrial fibrosis.American journal of physiology. Heart and circulatory physiology · 2026Article
- Inflammatory and hormonal crosstalk linking rheumatic fever to chronic valvular heart disease.Molecular biology reports · 2026Review
- Article
- Ubiquitination of Smad2 by Smurf1 inhibits endothelial-to-mesenchymal transition in human coronary artery endothelial cells.Scientific reports · 2026Article
- Construction of a risk scoring model based on machine learning and validation of the role of the key gene SERPINE1 in the progression of colon cancer.Cancer cell international · 2026Article
- Sex-Dependent Effects of Angiotensin II and Calcineurin in the Vasculature of Mice.Acta physiologica (Oxford, England) · 2026Article
- Variant-to-function dissection of the 17q21.31 locus resolves ANKRD1 as a convergent regulatory target.BMC medical genomics · 2026Article
- Advances in multi-omics and aging clock research for female reproductive health and aging.MedScience · 2026Review
- Estriol attenuates visceral adiposity and pulmonary artery smooth muscle cell proliferation via ERα-mediated signalling.European heart journal open · 2026Article
- The central role of IL-6 in the differential effects of GLP-1 receptor agonists and metformin across multiple health conditions.Frontiers in immunology · 2026Review
- Protective Effects of Estradiol on Disease Progression in a Murine Model of Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Loss of BPTF restores estrogen response and suppresses metastasis of mammary tumors.Nature communications · 2025Article
- CHIP mediates glucagon action on hepatic glucose production via regulating Smad3 ubiquitination.Diabetes, obesity & metabolism · 2025Article
- The untapped potential of radiation and immunotherapy for hormone receptor-positive breast cancer.NPJ breast cancer · 2025Review
- Single nucleus RNA-seq reveals the process from onset to chronic kidney disease in IgA nephropathy.Scientific reports · 2025Article
- Biological Aging and Uterine Fibrosis in Cattle: Reproductive Trade-Offs from Enhanced Productivity.Cells · 2025Review
- Estrogen attenuates stiffness-driven fibrotic signaling via transcriptional regulation.Biophysical journal · 2025Article
- Sex- and age-dependent neurovascular abnormalities linked to neuroinflammation lead to exacerbated post-ischemic brain injury in Marfan syndrome mice.Redox biology · 2025Article
- The Pathophysiology of Sex Differences in Stroke Risk and Prevention in Atrial Fibrillation: A Comprehensive Review.Medicina (Kaunas, Lithuania) · 2025Review
46 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
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen is a growth factor that stimulates cell proliferation. The effects of estrogen are mediated through the estrogen receptors, ERalpha and ERbeta, which function as ligand-induced transcription factors and belong to the nuclear receptor superfamily. On the other hand, TGF-beta acts as a cell growth inhibitor, and its signaling is transduced by Smads. Although a number of studies have been made on the cross-talk between estrogen/ERalpha and TGF-beta/Smad signaling, whose molecular mechanisms remain to be determined. Here, we show that ERalpha inhibits TGF-beta signaling by decreasing Smad protein levels. ERalpha-mediated reductions in Smad levels did not require the DNA binding ability of ERalpha, implying that ERalpha opposes the effects of TGF-beta via a novel non-genomic mechanism. Our analysis revealed that ERalpha formed a protein complex with Smad and the ubiquitin ligase Smurf, and enhanced Smad ubiquitination and subsequent degradation in an estrogen-dependent manner. Our observations provide new insight into the molecular mechanisms governing the non-genomic functions of ERalpha.
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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.