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Figure 8


Fig. 8. Working model for the NER-dependent H2AX phosphorylation in G0/G1-arrested human cells. Two distinct but partially overlapping pathways can be activated by UV or NA-AAF: one is a replication stress-induced pathway in cycling S-phase cells (Ward and Chen, 2001; Ward et al., 2004) and the other is a NER-mediated pathway in quiescent cells (this study). In both pathways ATR is the principal kinase for the H2AX phosphorylation and RPA seems to play a role in the recruitment of ATR-ATRIP. A major difference between the two pathways is in how RPA-coated ssDNA regions are generated. The NER-mediated ssDNA gaps or their processed products might be caused by perturbed repair synthesis because of extremely low levels of replication factors including Pol {delta}, Pol {epsilon} and PCNA (shown in grey).





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