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. 2015 Feb 6;14(3):342–353. doi: 10.4161/15384101.2014.987614

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Figure 3. — FANCD2^K561R binds chromatin and promotes restart of APH-stalled replication forks. (A) FANCD2-deficient cells (PD20) complemented with either empty vector, FANCD2^WT or FANCD2^K561R were either untreated or treated with APH, and analyzed for FANCD2 and FANCD2^Ub. Ku-86, loading control. (B) The 3 cell types described in (A) were either untreated or treated with APH for 6h or 24h, and chromatin fractions from the cells were analyzed for the presence of FANCD2 and FANCD2^Ub. Ku-86, loading control. (C) Replication fork restart efficiencies after APH treatment were compared between the 3 cell types described in (A). (D) The number of new replication sites originating during BioU labeling after APH treatment was compared between the 3 cell types described in (A).