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. 2010 May 3;189(3):445–463. doi: 10.1083/jcb.200909175

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© 2010 Luijsterburg et al.

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Figure 6. — Random and reversible NER complex assembly accounts both for rapid exchange and prolonged net accumulation of repair proteins. (A–D) Comparison of model simulations (lines) and experimental data (dots) showing net accumulation kinetics (A) and dissociation kinetics (B) of core NER proteins, dissociation kinetics of XPC in wild-type and XPF-deficient cells unable to perform damage excision (C), and dissociation kinetics of XPA and PCNA in the absence or presence of DNA synthesis/ligation inhibitors HU and AracC (D). (E) Affinity of NER proteins for the repair intermediates (K_a = k_on/k_off). Preincision factors XPG, TFIIH, and ERCC1/XPF lose affinity after lesion excision, whereas the affinities of XPA, PCNA, and RPA increase upon repair synthesis. (F) Computed time courses of the repair intermediates. Note that the color coding of the repair intermediates, as indicated in E, also applies to F. (G) Comparison between the predicted kinetics of the removal of 6-4 PPs (blue) and the measurements on the kinetics of 6-4 PP removal by means of quantitative immunostaining using specific antibodies (red). Between 50 and 70 cells were analyzed for each time point. Error bars indicate SD.