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. Author manuscript; available in PMC: 2012 Jan 2.
Published in final edited form as: DNA Repair (Amst). 2010 Oct 13;10(1):5–15. doi: 10.1016/j.dnarep.2010.09.004

Figure 2.

Figure 2

Figure 2

Phosphorylation of histone H2AX, ATM and Nbs1 after exposure to uniform UV in XP-B cells. A. Normal (0.8 μm beads – red arrows) and XP-B cells (2.0 μm beads – yellow arrows) on the same slide were irradiated with 10 J/m2 UV and then cultured for various periods of time before fixation. Immunofluorescent double labeling was performed. γ-H2AX, p-ATM and p-Nbs1 persisted for more than 24 h in XP-B but not normal cells. B. Quantification of phosphorylated histone H2AX, ATM and Nbs1 after exposure to UV at various post-UV irradiation intervals. The levels of γ-H2AX, p-ATM and p-Nbs1 were increased by 6 h after 10 J/m2 UV irradiation and persisted for more than 24 h in XP-B but not normal cells. C. Increased UV-induced phosphorylation of H2AX in XP-B cells by Western blotting. D. Increased Wip1 level in normal but not in XP-B fibroblasts following exposure to UV detected by Western blotting. E. Post-UV cell viability of normal and XP-B cells. Normal (AG13145) and XP-B (XP183MA and XP33BR) cells were treated with 10 J/m2 UV and cultured for up to 4 days. Cell viability was assessed using MTS assay. The XP-B cells had reduced post-UV cell viability at all time points tested.