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. Author manuscript; available in PMC: 2009 Jan 1.
Published in final edited form as: Mol Pharmacol. 2007 Oct 19;73(1):260–269. doi: 10.1124/mol.107.041764

Fig. 4.

Fig. 4

HMGB1 contributes to activation of p53 target genes in response to genotoxic stress. Hmgb1+/+ and Hmgb1−/− MEFs were transfected with luciferase reporter plasmids driven by p21, Bax, Puma, and Noxa promoters, or control plasmid, and treated with 10 μM MP (upper panel) or 0.5 μM araC (lower panel). Trans-activation of p53-regulated promoters p21, Bax, Puma, and Noxa in MEFs was normalized by constitutively expressed Renilla luciferase activity. Activity of Puma and Noxa promoters was significantly different in two cell lines after MP treatment; and activity of Bax, Puma, and Noxa promoters was significantly different after araC treatment (p<0.05). Results of experiments are depicted as fold change of promoter activity relative to cells untreated with genotoxic drugs. Data are expressed as the mean ± S.D. of three independent experiments. Asterisks denote significantly different levels of activity (p<0.05). Bars, SD. ru, relative units.