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• W2086985369 abstract "Thyroid hormone (T3) mediates diverse physiological functions including growth, differentiation, and energy homeostasis through the thyroid hormone receptors (TR). The TR binds DNA at specific recognition sequences in the promoter regions of their target genes known as the thyroid hormone response elements (TREs). Gene expression at TREs regulated by TRs is mediated by coregulator recruitment to the DNA bound receptor. This TR-coregulator interaction controls transcription of target genes by multiple mechanisms including covalent histone modifications and chromatin remodeling. Our previous studies identified a β-aminoketone as a potent inhibitor of the TR-coactivator interaction. We describe here the activity of one of these inhibitors in modulating effects of T3 signaling in comparison to an established ligand-competitive inhibitor of TR, NH-3. The β-aminoketone was found to reverse thyroid hormone induced gene expression by inhibiting coactivator recruitment at target gene promoters, thereby regulating downstream effects of thyroid hormone. While mimicking the downstream effects of NH-3 at the molecular level, the β-aminoketone affects only a subset of the thyroid responsive signaling network. Thus antagonists directed to the coregulator binding site have distinct pharmacological properties relative to ligand-based antagonists and may provide complementary activity in vivo." @default.
• W2086985369 created "2016-06-24" @default.
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• W2086985369 date "2011-08-15" @default.
• W2086985369 modified "2023-09-26" @default.
• W2086985369 title "Similarities and Differences between Two Modes of Antagonism of the Thyroid Hormone Receptor" @default.
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• W2086985369 doi "https://doi.org/10.1021/cb200092v" @default.
• W2086985369 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3199310" @default.
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