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. Author manuscript; available in PMC: 2016 Oct 26.
Published in final edited form as: Cancer Res. 2012 Jan 26;72(6):1529–1537. doi: 10.1158/0008-5472.CAN-11-2602

Figure 3.

Figure 3

PTPN1 is a direct target of the AR. (A) Sequence logo depicting a GRE sequence enriched in AR-bound segments identified by ChIP-on-chip obtained following a de novo motif discovery. (B) Binding profile of AR from the ChIP-on-chip performed with LNCaP cells on a high-resolution tiled array covering PTPN1 and its vicinity (N=2). (C and D) Standard ChIP in LNCaP cells shows that (C) AR is recruited to the 6 kb (Kruskal-Wallis test, p<0.05) and 28 kb enhancers (Kruskal-Wallis test, near to significance, p=0.075) upon R1881 treatment. We also observed a slight but non-significant increase in AR recruitment at the TSS (Kruskal-Wallis test, p<0.05). AR binding at these sites was abrogated when cells were pretreated with BIC (Representative experiment, N=2 +/− SEM). (D) RNAPol II occupancy at the TSS is increased after treatment with R1881 (Kruskal-Wallis test, p<0.05) but not when cells where pretreated with BIC (Representative experiment, N=2 +/− SEM).