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. 2014 Jan 21;5(4):959–969. doi: 10.18632/oncotarget.1360

Figure 2. Inhibition of AR activity by the engineered repressors.

Figure 2

(a) COS-1 cells were transiently transfected with vectors for the AR, TAT-GRE-E1B-LUC, PDM-LACZ-β-GAL and the repressors or interaction motif either in isolation (solid line) or as a fusion (broken line). (b) PC3-WTAR were transiently transfected with vectors for TAT-GRE-E1B-LUC, PDM-LACZ-β-GAL, AR1-54 or the repressors. (c) COS-1 cells were transfected with vectors encoding the androgen, glucocorticoid, oestrogen or progesterone receptors (AR, GR, ER, PR), the respective luciferase reporter construct (TAT-GRE-E1B-LUC or ERE-LUC), PDM-LACZ-β-GAL and PLZF1-452-AR1-54. Luciferase activity was normalised with β-galactosidase expression and results expressed as a % of AR activity in the absence of the repressors. Mean of 3 independent duplicates ±1SE. T-Test - **p<0.005, ***p<0.0005