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. Author manuscript; available in PMC: 2007 Dec 28.
Published in final edited form as: Mol Cell. 2006 Dec 28;24(6):841–851. doi: 10.1016/j.molcel.2006.11.026

Figure 5. p53-(K120R) is specifically defective for BAX and PUMA induction.

Figure 5

(A) H1299-p53ER and –p53ER-(K120R) cells were treated with 50 or 100 nM 4-OHT or vehicle for 24 hours. Cells were collected, lysed and subjected to western blot with the antibodies indicated. (B) H1299-p53ER and –p53ER-(K120R) cells were treated with 50 or 200nM 4-OHT for 24 hours and subsequently harvested for RNA at 0, 6, 12, 18 and 24 hours. cDNA generated from recovered RNA was amplified with primers to the target genes indicated and quantified by real-time PCR. (C) H1299-p53ER and –p53ER-(K120R) cells were treated with 100nM 4-OHT or vehicle for 6 hours. Cells from each condition were cross-linked and subjected to ChIP analysis with a p53 antibody. Precipitated DNA was recovered and analyzed by real-time PCR with primers that amplify the p53-binding site within the BAX, PUMA, hMDM2, and p21 promoters. Error bars represent standard deviation of three independent reactions.