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Updated: Aug 25, 2026

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
Published on: September 20, 2018
Modifying chromatin to permit steroid hormone receptor-dependent transcription
H Karimi Kinyamu1, Trevor K Archer
1Chromatin and Gene Expression Section, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, PO Box 12233 (MD E4-06), Research Triangle Park, NC 27709, USA.
Abstract:
Lipophilic hormones, including steroids, exert their physiological effects through binding to high-affinity superfamily of steroid hormone receptor (SR) proteins that function as ligand-dependent DNA binding transcription factors. To date, SR proteins are among a few transcription factors shown to directly interact with higher order chromatin structures to regulate gene expression. To perturb chromatin, SRs employ enzymatic multicomplexes that can either remodel or modify chromatin. Here we examine the current state of knowledge concerning multicomplex chromatin remodeling/modification machines and SR-dependent transcription. We will focus on the role of these protein-protein and chromatin-protein interactions in vivo with the MMTV promoter as a primary model. In addition, we discuss emerging evidence implicating chaperone proteins and proteasome degradation machinery in SR-mediated gene regulation within chromatin.
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