A p53-derived apoptotic peptide derepresses p73 to cause tumor regression in vivo
J. Clin. Invest. Helen S. Bell, et al. 117:1008 doi:10.1172/JCI28920 [Go to this article.]

Figure 1
The p53-derived peptide 37AA induces cell death without direct activation of p53 target genes. (A) Representation of the p53 mutants used in this study. Full-length p53 is shown in green with 5 evolutionarily conserved regions (boxes) shown in yellow. Two truncations, tr105 (aa 1–105) and tr210 (aa 1–210), are shown as well as the composition of the 37AA peptide, with aa from conserved box II (residues 118–142) in red and those from conserved box III (residues 171–181) in blue. (B–E) Cells were transiently transfected with the indicated plasmids and subsequently analyzed 36 hours (C and E) and 48 hours later (D) for changes in cell cycle and cell death by flow cytometry. Ap, apoptosis. (B) Cells were transiently transfected with the indicated plasmids, and transgene expression was determined by Western blotting. The additional lower band seen following expression of 37AA represents expression from an alternate internal methionine. Mutation of this methionine to alanine resulted in expression of the larger protein species only and produced identical results (not shown). (F) No direct activation of p53 target genes by 37AA was observed. Saos-2 cells were transfected with luciferase reporter plasmids for the p53 target genes p21, Bax, and PIG3 as well as with the indicated expression constructs. After 24 hours, cells were assayed for luciferase activity, and the data were normalized against transfected β-gal activity. Values represent fold activation relative to activity of GFP alone, which was assigned as 1.