<p><b>Copyright information:</b></p><p>Taken from "The zinc finger domain of Wilms' tumor 1 suppressor gene (WT1) behaves as a dominant negative, leading to abrogation of WT1 oncogenic potential in breast cancer cells"</p><p>http://breast-cancer-research.com/content/9/4/R43</p><p>Breast cancer research : BCR 2007;9(4):R43-R43.</p><p>Published online 16 Jul 2007</p><p>PMCID:PMC2206716.</p><p></p> Schematic drawing for luciferase reporter constructs. The predominant transcription start site (+1) is indicated by an arrow. Small solid triangles indicate Wilms' tumor 1 suppressor gene (WT1) binding sites. MCF-7 cells and MDA468 cells were co-transfected with plasmids expressing the WT1 proteins (either pcDNAcontrol (CON), aminoterminal-only construct N-WT1, zinc finger domain lacking or with lysine–threonine–serine (ZF - KTS or ZF + KTS) or full-length WT1 vectors A~D), and either the pGL2 vector control or the differential WT1 promoter-driven luciferase constructs (horizontal axis), respectively. Luciferase activity was normalized with β-galactosidase activity and is expressed in relative luciferase activity as compared with the luciferase vector control (vertical axis). Results are the average of three experiments
