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Steroid hormone receptors silence genes by a chromatin-targeted mechanism similar to those used for gene activation

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Pages 15-20 | Received 06 Sep 2016, Accepted 23 Sep 2016, Published online: 20 Oct 2016

Figures & data

Figure 1. Model of gene repression induced by progestins in breast cancer cells. At uninduced conditions, genes are active with RNA pol II and an open chromatin configuration characterized by the presence of the pioneer factor FOXA1 and acetylated histones. Upon hormone exposure, activated PR along with the HP1γ–LSD1.com complex interacts with the ATPase BRG1 and promotes histone deacetylation, demethylation, and chromatin remodeling via BRG1, which increase nucleosome positioning and occupancy. This arrangement of nucleosomes constitutes a suitable platform for histone H1.2 binding, and thus close the target chromatin decreasing RNApol II loading and transcription.

Figure 1. Model of gene repression induced by progestins in breast cancer cells. At uninduced conditions, genes are active with RNA pol II and an open chromatin configuration characterized by the presence of the pioneer factor FOXA1 and acetylated histones. Upon hormone exposure, activated PR along with the HP1γ–LSD1.com complex interacts with the ATPase BRG1 and promotes histone deacetylation, demethylation, and chromatin remodeling via BRG1, which increase nucleosome positioning and occupancy. This arrangement of nucleosomes constitutes a suitable platform for histone H1.2 binding, and thus close the target chromatin decreasing RNApol II loading and transcription.

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