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. Author manuscript; available in PMC: 2015 Jul 15.
Published in final edited form as: J Immunol. 2014 Jun 16;193(2):931–939. doi: 10.4049/jimmunol.1400002

Figure 7. The reduction in germinal center size is p53-dependent.

Figure 7

Germinal center formation is partially restored in APE2-deficient mice that are also deficient in p53. (A) FACS plot showing the percent of PP GC cells in mice of the indicated genotypes (representative of 3 independent experiments). (B) Partial recovery in the number of GC cells in apex2Y/− x tp53−/− mice (WT and APE2, n=3; p53 and APE2xp53, n=4; *p < 0.05 vs. WT; n.s., not significant). (C) qRT-PCR shows increased expression of the p53-dependent pro-apoptotic gene bax relative to HPRT expression in APE2-deficient FACS-purified PP GC B cells (mean ± SEM, n=3 independent sorts). (D) APE2-deficient B220+GL7+CXCR4HI centroblasts show a cell cycle block that is not dependent on p53 (representative FACS profile with mean ± SEM, n=3, except p53 n=2 and range is shown).