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. 2016 Jun 7;10(8):1207–1220. doi: 10.1016/j.molonc.2016.05.007

Figure 4.

Figure 4

K120R binding is enhanced at TNFAIP8 locus. (A) TO‐p53 cells (WT or K120R) were treated with tetracycline or not treated, then harvested after 24 h. After crosslinking, cell lysates were subject to chromatin immunoprecipitation (ChIP) with antibody for p53, and purified DNA was sequenced and processed. Peaks for p53 at TNFAIP8, CDKN1A and Bax loci are shown, visualized using the UCSC Genome Browser. Peak scale is indicated to the left of the panel for each gene in normalized reads. (B) qRT‐PCR of RNA extracted from cells used in ChIP‐Seq experiment measuring transcript levels of CDKN1A, Bax and TNFAIP8. Values were normalized to GAPDH. Error bars indicate ± S.D. (C) p53 ChIP signal on DNA extracted from cells treated as described in (A) relative to input DNA at TNFAIP8 locus (+500 bp) for WT and K120R, −/+ Tet. Error bars indicate ± S.D. (D) Western blot for p53 and actin control from cells used to generate ChIP‐Seq data.