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. Author manuscript; available in PMC: 2013 Mar 11.
Published in final edited form as: J Biol Chem. 2008 Jan 8;283(11):6687–6695. doi: 10.1074/jbc.M705606200

FIGURE 3. Expression of dominant negative JNK1 alters AP-1 transcriptional activation and liver injury in a JunD-dependent manner following I/R.

FIGURE 3

JunD−/− and JunD+/− mice were infected (intravenously) with Ad.AP-1Luc and either Ad.LacZ or Ad.dnJNK1 viruses 3 days prior to I/R injury (partial lobar ischemia for 45 min followed by the indicated times of reperfusion). A and B, serum GPT levels; C and D, luciferase activities in liver lysates were assessed at the indicated time points, for each vector combination and JunD genotype, as indicated. Results depict the mean (± S.E.) for n = 3 animals at each experimental point. The 0-h time point represents non-I/R-injured control animals. E, 5-bromo-4-chloro-3-indolyl-β-D-galactopyranoside (X-gal)-stained liver section detecting β-galactosidase activity from uninfected and Ad.LacZ-infected mice.