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. Author manuscript; available in PMC: 2009 Jan 6.
Published in final edited form as: Cancer Lett. 2006 Jan 18;242(2):207–214. doi: 10.1016/j.canlet.2005.11.007

Figure 1. Smad/Smad binding element (SBE) DNA binding activity.

Figure 1

(A) The protein/DNA array was performed using nuclear extracts from SK-N-SH cells treated with vehicle (control) or LY294002 (20 μM), a PI3-K inhibitor. Signals outlined in boxes represent activated Smad/SBE by LY294002 treatment. (B) Nuclear protein was assayed for Smad/SBE DNA binding with a biotin-labeled oligonucleotide containing the Smad/SBE consensus sequence (AGTATGTCTAGACTGA). LY294002 treatment significantly increased DNA binding (lane 3). Treatment with wortmannin, another PI3-K inhibitor, also increased Smad/SBE DNA binding (lane 6). Competition experiments were performed with a 30-fold molar excess of the unlabeled Smad/SBE oligonucleotide.