Estrogen Receptor α Mediates 17α-Ethynylestradiol Causing Hepatotoxicity*

@article{Yamamoto2006EstrogenR,
  title={Estrogen Receptor $\alpha$ Mediates 17$\alpha$-Ethynylestradiol Causing Hepatotoxicity*},
  author={Yukio Yamamoto and Rick Moore and Holly A Hess and Grace L. Guo and Frank J. Gonzalez and Kenneth S. Korach and Robert R. Maronpot and Masahiko Negishi},
  journal={Journal of Biological Chemistry},
  year={2006},
  volume={281},
  pages={16625 - 16631}
}
Estrogens are known to cause hepatotoxicity such as intrahepatic cholestasis in susceptible women during pregnancy, after administration of oral contraceptives, or during postmenopausal replacement therapy. Enterohepatic nuclear receptors including farnesoid X receptor (FXR), pregnane X receptor (PXR), and constitutive active/androstane receptor (CAR) are important in maintaining bile acid homeostasis and protecting the liver from bile acid toxicity. However, no nuclear receptor has been… 

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TLDR
Analysis of metabolic changes induced by EE in livers from hypophysectomized (HYPOX) and hypothyroid rats shows that pituitary hormones play a critical role in the hepatic effects of EE, and demonstrates a novel mechanism of action of EE through binding and negative regulation of glucocorticoid receptor-mediated transcription.
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TLDR
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TLDR
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TLDR
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Hepatotoxicity induced by neonatal exposure to diethylstilbestrol is maintained throughout adulthood via the nuclear receptor SHP
TLDR
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