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. 2008 May 27;105(22):7785–7790. doi: 10.1073/pnas.0703423105

Fig. 1.

Fig. 1.

p53 accumulates in AT cells in response to IR. (A) Lymphoblasts from AT patients (719; 1526; and 3189), from a patient with Nijmegen breakage syndrome (NBS), and from an unaffected control were probed for ATM and for proliferating cell nuclear antigen (PCNA) for loading control. (B) Lymphoblasts from AT patients and an unaffected control were irradiated, harvested at the indicated time points, and probed for p53 and for PCNA for loading control. (C) Lymphoblasts from AT patients and an unaffected control were irradiated with the indicated doses, harvested 4 h after irradiation, and probed for p53 and PCNA. (D) Lymphoblasts from AT patients and an unaffected control were incubated in the presence of 10 μM MG132 for 4 h. Fifteen, 30, or 60 min before harvest, cells were irradiated, lysed, and probed for p53 phosphorylated at serine-15, serine-20, pan-p53, and PCNA. (E) Wild-type lymphoblasts were incubated with 10 μM MG132 for 5 h or left untreated for control. Thirty minutes before irradiation an ATM kinase inhibitor (10 μM) was added. Cells were lysed 1.5 h after irradiation and probed for p53 and PCNA. Lysates from cells that had been incubated with MG132 were also probed for p53 phosphorylated at serine-15.