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. Author manuscript; available in PMC: 2012 Aug 9.
Published in final edited form as: Oncogene. 2011 Jul 18;31(6):716–727. doi: 10.1038/onc.2011.273

Figure 3. Vav3 increases androgen-induced AR N-C interaction in a PH dependent but GEF independent manner.

Figure 3

A. Schematic shows Vav3 domain organization and the Vav3 PH and GEF mutants. B. Mammalian two hybrid assays were conducted in which PC3 cells transfected with plasmids encoding: VP16AD-ARTAD [the VP16 activation domain (AD) fused to AR amino acids 1–565], Gal4DBD-ARLBD [the Gal4 DNA binding domain (DBD) fused to the AR ligand binding domain (LBD) 628–919], Gal4-Tata-Luc, and empty vector (EV), Vav3, Vav3 PH mutant W493L or Vav3 GEF mutant (ISO) were treated with either vehicle or R1881 for 24h. Samples were then assayed for luciferase activity and normalized to protein concentration. Data plotted as RLU relative to EV with vehicle treatment (± SEM) are averaged from 3–8 independent experiments. Significance was determined by two-tailed Student’s t test comparing EV transfected cells with R1881 (1 nM) treatment (**p<0.01,*p<0.05). C. Western blot of parallel cultures transfected with indicated plasmids shows expression of Vav3 and Vav3 mutants.