Transcriptional Regulation of the Human NRIP1/RIP140 Gene by Estrogen Is Modulated by Dioxin Signalling (original) (raw)
Negative regulation of hormone signaling by RIP140
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The Transcription Factor Aryl Hydrocarbon Receptor Nuclear Translocator Functions as an Estrogen Receptor Selective Coactivator, and Its Recruitment to Alternative Pathways Mediates Antiestrogenic Effects of Dioxin
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The Transcription Factor Aryl Hydrocarbon Receptor Nuclear Translocator Functions as an Estrogen Receptor β-Selective Coactivator, and Its Recruitment to Alternative Pathways Mediates Antiestrogenic Effects of Dioxin
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The transcription factor aryl hydrocarbon receptor nuclear translocator functions as an estrogen receptor beta-selective coactivator, and its recruitment to alternative pathways mediates antiestrogenic effects of dioxin
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Receptor-Interacting Protein 140 Differentially Regulates Estrogen Receptor-Related Receptor Transactivation Depending on Target Genes
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RIP 140 enhances nuclear receptor-dependent transcription in vivo in yeast
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RIP140 Expression Is Stimulated by Estrogen-related Receptor during Adipogenesis
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RIP-140 interacts with multiple nuclear receptors by means of two distinct sites
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ERα-AHR-ARNT Protein-Protein Interactions Mediate Estradiol-dependent Transrepression of Dioxin-inducible Gene Transcription
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Distinct functions for RIP140 in development, inflammation, and metabolism
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Alternative Pathways Mediates Antiestrogenic Effects of Dioxin to Functions as an Estrogen Receptor ²Selective Coactivator, and Its Recruitment The Transcription Factor Aryl Hydrocarbon Receptor Nuclear Translocator
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Xenoestrogens down-regulate aryl-hydrocarbon receptor nuclear translocator 2 mRNA expression in human breast cancer cells via an estrogen receptor alpha-dependent mechanism
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Estrogen receptor � acts as a dominant regulator of estrogen signaling
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Analysis of Estrogen Receptor Interaction with a Repressor of Estrogen Receptor Activity (REA) and the Regulation of Estrogen Receptor Transcriptional Activity by REA
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