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. 2008 Apr 3;36(9):2969–2980. doi: 10.1093/nar/gkn132

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© 2008 The Author(s)

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Recruitment of p63γ protein to the S100A2 promoter may connect S100A2 expression to DNA damage. (A) TAp63γ and S100A2 mRNA expression increase after DNA damage. Real-time RT–PCR measurements of S100A2 and TAp63 mRNAs from doxorubicin-treated HepG2 cells. Relative mRNA levels were normalized to expression of GAPDH mRNA. Cells before treatment were employed as control. Control levels were set to 100%. Times of doxorubicin treatment are indicated. (B) Western blot analyses of lysates from p53-positive HepG2 and p53-negative Hep3B cells after doxorubicin-induced DNA damage. Controls contain samples taken before treatment. Doxorubicin-treated samples were analyzed after 24 h or 48 h. Detection of β-actin served as a loading control. (C) Expression of S100A2 mRNA correlates with an increase of TAp63 mRNA after doxorubicin-induced DNA damage in p53-negative Hep3B cells. Relative mRNA levels were measured by real-time RT–PCR. Expression of GAPDH was used for normalization. S100A2 mRNA from untreated control cells was set to 100%. In control samples no TAp63 mRNA was detectable. Therefore, the TAp63 mRNA measurement at 24 h was employed as the 100% reference. (D) Chromatin immunoprecipitation (ChIP) assays of p53 and p63γ proteins binding to the S100A2 promoter in HepG2 cells following DNA damage. Control and doxorubicin-treated cells were prepared as described above. Lanes are input (i), no antibody (n), p53 and p63γ antibodies.