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. Author manuscript; available in PMC: 2009 Feb 13.
Published in final edited form as: Mol Cell Endocrinol. 2007 Nov 17;283(1-2):19–31. doi: 10.1016/j.mce.2007.10.014

Figure 3. Binding of GR to GREs releases pre-existing INHAT complex from GREs via physical interaction between the GR and Set/TAF-Iβ.

Figure 3

A: Ligand-activated GR releases INHAT components Set/TAF-Iβ and pp32 from the MMTV GREs in HCT116/MMTV cells (left panels) and TAT GREs in HTC cells (right panels)

HCT116/MMTV cells transfected with pRShGRα or the control plasmid and HTC cells were treated with 10−6 M of dexamethasone (Dex). They were fixed with 1% formaldehyde and ChIP assays were performed by using anti-Set/TAF-Iβ, anti-pp32, anti -GRα or control antibodies.

B: Ligand-activated GR releases the wild type Set/TAF-Iβ but not the GR-binding domain-defective Set/TAF-Iβ-(Δ181–225) from the MMTV-GREs in HCT116/MMTV cells.

HCT116/MMTV cells were transfected with His-Set/TAF-Iβ-expressing plasmids and/or pRShGRα. The cells were treated with 10−6 M of dexamethasone (Dex), fixed with 1% formaldehyde and ChIP assays were performed by using anti-His, anti-GRαor control antibodies.

C: Overexpression of Set/TAF-Iβ-(181–225) attenuates GR-induced release of Set/TAF-Iβ from GREs in HCT116/MMTV cells. HCT116/MMTV cells were transfected with 0.5 μg/well of His-Set/TAF-Iβ-expressing plasmid (as “1”), pRShGRα and the indicated amounts (ratios) of the Set/TAF-Iβ-(Δ181–225)-expressing plasmid. The cells were treated with 10−6 M of dexamethasone (Dex), fixed with 1% formaldehyde and ChIP assays were performed using anti-His, anti-GRαor control antibodies.