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. 2012 Jun 28;7(6):e39586. doi: 10.1371/journal.pone.0039586

Figure 3. Loss of Puma but not p53, protects against tunicamycin-induced cell death and caspase-3 activation.

Figure 3

(A) PUMA-deficient telencephalic neurons exhibited significantly less death after exposure to tunicamycin in comparison to wild-type telencephalic neurons from litter mate controls. Similarly, PUMA-deficient telencephalic neurons were protected against AraC-induced cell death (B) PUMA-deficient telencephalic neurons exhibited a significant attenuation in caspase-3 activation after exposure to tunicamycin or AraC in comparison to wild-type neurons. (C) p53-deficient telencephalic neurons did not exhibit significant protection against tunicamycin-induced cell death although they were protected from AraC-induced cell death in comparison to wild-type telencephalic neurons. (D) p53-deficient telencephalic neurons exhibited a significant attenuation in caspase-3 activation after exposure to AraC in comparison to wild-type litter control neurons but not after treatment with tunicamycin. (E) BIM-deficient telencephalic neurons demonstrated no significant protection against tunicamycin-induced cell death in comparison to wild-type littermates. The data represent mean ± SEM, with n = 5. *p<0.01 by two-way ANOVA/Bonferroni post hoc test compared to both the wild-type and the knock-out treated group.