Low doses of bisphenol A promote human seminoma cell proliferation by activating PKA and PKG via a membrane G-protein-coupled estrogen receptor.
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Gene expression in the fetal mouse ovary is altered by exposure to low doses of bisphenol ABiological Tools to Study the Effects of Environmental Contaminants at the Feto-Maternal InterfaceEffects of Endocrine-Disrupting Chemicals on the OvaryGPER Signaling in Spermatogenesis and Testicular TumorsNon-monotonic dose-response relationships and endocrine disruptors: a qualitative method of assessmentA structural view of nuclear hormone receptor: endocrine disruptor interactionsImpacts of environmental toxicants on male reproductive dysfunctionAssessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge aheadBisphenol A accelerates capacitation-associated protein tyrosine phosphorylation of rat sperm by activating protein kinase AHigh-Content Analysis Provides Mechanistic Insights into the Testicular Toxicity of Bisphenol A and Selected Analogues in Mouse Spermatogonial CellsRapid insulinotropic action of low doses of bisphenol-A on mouse and human islets of Langerhans: role of estrogen receptor βDifferential effects of bisphenol A and diethylstilbestrol on human, rat and mouse fetal leydig cell functionNuclear receptors and endocrine disruptors in fetal and neonatal testes: a gapped landscape.Developmental exposure of mice to dioxin promotes transgenerational testicular inflammation and an increased risk of preterm birth in unexposed mating partners.A clash of old and new scientific concepts in toxicity, with important implications for public healthEarly embryonic androgen exposure induces transgenerational epigenetic and metabolic changes.Bisphenol A at concentrations relevant to human exposure enhances histamine and cysteinyl leukotriene release from bone marrow-derived mast cells.Non-monotonic dose responses in studies of endocrine disrupting chemicals: bisphenol a as a case studyBisphenol A activates Maxi-K (K(Ca)1.1) channels in coronary smooth muscleNongenomic signaling pathways of estrogen toxicity.Is it time to end concerns over the estrogenic effects of bisphenol A?GPR30, the non-classical membrane G protein related estrogen receptor, is overexpressed in human seminoma and promotes seminoma cell proliferation.Low concentrations of o,p'-DDT inhibit gene expression and prostaglandin synthesis by estrogen receptor-independent mechanism in rat ovarian cells.Endocrine disruptors, environmental oxygen, epigenetics and pregnancyBisphenol A modulates calcium currents and intracellular calcium concentration in rat dorsal root ganglion neurons.An alkylphenol mix promotes seminoma derived cell proliferation through an ERalpha36-mediated mechanism.Endocrine disrupting chemicals and disease susceptibility.Chronic oral exposure to bisphenol A results in a nonmonotonic dose response in mammary carcinogenesis and metastasis in MMTV-erbB2 miceLow concentrations of bisphenol A induce mouse spermatogonial cell proliferation by G protein-coupled receptor 30 and estrogen receptor-α.17β-estradiol signaling and regulation of Sertoli cell functionEndocrine disrupting chemicals: Multiple effects on testicular signaling and spermatogenesis.Bisphenol A induces gene expression changes and proliferative effects through GPER in breast cancer cells and cancer-associated fibroblasts.Non-genomic effects of xenoestrogen mixtures.Bisphenol A and Related Alkylphenols Exert Nongenomic Estrogenic Actions Through a G Protein-Coupled Estrogen Receptor 1 (Gper)/Epidermal Growth Factor Receptor (Egfr) Pathway to Inhibit Meiotic Maturation of Zebrafish OocytesMolecular mechanism(s) of endocrine-disrupting chemicals and their potent oestrogenicity in diverse cells and tissues that express oestrogen receptorsMolecular mechanisms underlying the rapid arrhythmogenic action of bisphenol A in female rat hearts.Molecular pathways: environmental estrogens activate nongenomic signaling to developmentally reprogram the epigenome.Environmental estrogens differentially engage the histone methyltransferase EZH2 to increase risk of uterine tumorigenesis.Genetic variants of GPER/GPR30, a novel estrogen-related G protein receptor, are associated with human seminoma.Trends in incidence and survival of pediatric and adolescent patients with germ cell tumors in the United States, 1975 to 2006.
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P2860
Low doses of bisphenol A promote human seminoma cell proliferation by activating PKA and PKG via a membrane G-protein-coupled estrogen receptor.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 11 February 2009
@en
vedecký článok
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vetenskaplig artikel
@sv
videnskabelig artikel
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vědecký článek
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name
Low doses of bisphenol A promo ...... ein-coupled estrogen receptor.
@en
Low doses of bisphenol A promo ...... ein-coupled estrogen receptor.
@nl
type
label
Low doses of bisphenol A promo ...... ein-coupled estrogen receptor.
@en
Low doses of bisphenol A promo ...... ein-coupled estrogen receptor.
@nl
prefLabel
Low doses of bisphenol A promo ...... ein-coupled estrogen receptor.
@en
Low doses of bisphenol A promo ...... ein-coupled estrogen receptor.
@nl
P2093
P2860
P356
P1476
Low doses of bisphenol A promo ...... ein-coupled estrogen receptor.
@en
P2093
Adil Bouskine
Françoise Brücker-Davis
Marielle Nebout
Mohamed Benahmed
Patrick Fenichel
P2860
P304
P356
10.1289/EHP.0800367
P577
2009-02-11T00:00:00Z