Estradiol Repression of Tumor Necrosis Factor-α Transcription Requires Estrogen Receptor Activation Function-2 and Is Enhanced by Coactivators

The tumor necrosis factor-α (TNF-α) promoter was used to explore the molecular mechanisms of estradiol (E2)-dependent repression of gene transcription. E2inhibited basal activity and abolished TNF-α activation of the TNF-α promoter. The E2-inhibitory element was mapped to the -125 to -82 region of t...

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Veröffentlicht in:	Proceedings of the National Academy of Sciences - PNAS 1999-12, Vol.96 (26), p.15161-15166
Hauptverfasser:	An, Jinping, Ralff C. J. Ribeiro, Webb, Paul, Gustafsson, Jan-Ake, Kushner, Peter J., Baxter, John D., Leitman, Dale C.
Format:	Artikel
Sprache:	eng
Schlagworte:	Adaptor Proteins, Signal Transducing Binding Sites Biological Sciences Cell lines estradiol Estradiol - pharmacology Estrogen Receptor alpha Estrogen Receptor beta Estrogen Receptor Modulators - pharmacology Estrogens Gene Expression Regulation Genes Genetic mutation glucocorticoid receptor-interacting protein 1 Herpes simplex virus Hormones Ligands Medical research Mutation Necrosis Nuclear Proteins - metabolism Nuclear Receptor Coactivator 2 Nuclear Receptor Interacting Protein 1 Nuclear receptors p160 protein Promoter regions Proteins Receptors Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Repression Response Elements Selective Estrogen Receptor Modulators - metabolism Simplexvirus - enzymology Simplexvirus - genetics Thymidine Kinase - genetics Transcription Factor AP-1 - metabolism Transcription Factors - metabolism Transcription, Genetic - drug effects tumor necrosis factor-a Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - pharmacology Tumors
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