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. Author manuscript; available in PMC: 2015 May 27.
Published in final edited form as: Nat Commun. 2014 Nov 27;5:5567. doi: 10.1038/ncomms6567

Figure 4. The proline-rich domain of p53 affects DNA damage-induced cell death in airway epithelial cells.

Figure 4

(A) H1299p53tsArg and H1299p53tsPro cells treated with 50 ng/ml DRB, and either 1 µM doxorubicin, 10 µM cyclohexamide, or 1 µM thapsigargin, and cell numbers quantified 48 h later. (B) p53 levels were increased in p53WT and p53AXXA MEFs when treated with 10 mJ UV irradiation. (C) p53WT and p53AXXA MEFs treated with 10 mJ UV irradiation in the presence of 50 ng/ml DRB and cell death analyzed by Annexin V and propidium iodide (PI) staining. (D) Quantification of Annexin V-positive cells in p53WT and p53AXXA MEFs following treatment for 8 h with 50 ng/ml DRB and either 10 mJ UV irradiation, 1 µM doxorubicin, 5% O2 (hypoxia), 95% O2 (hyperoxia), or 1 µM thapsigargin. (E) Western blot verifying the presence of p53 after infection of p53WT and p53AXXA MEFs with adenoviral vectors expressing p53Arg or p53Pro. (F) p53WT and p53AXXA MEFs were either left untreated (control) or infected with adenoviral vectors for p53Arg or p53Pro then treated with 1µM doxorubicin for 24 h and cell numbers quantified. Bars = group means ± standard error from the mean (n = 3 different treatments/group) ; * P<0.05; ** P<0.01.