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. 2017 Dec 4;8(68):112942–112958. doi: 10.18632/oncotarget.22896

Figure 4. NEIL3 is associated at replication fork during replication stress and its loss impaired the recruitment of replication associated homologous repair proteins.

Figure 4

(A) The recruitment of NEIL3, Rad51, RPA, PCNA, and CHK1 after HU treatment at new synthesized DNA fragments; (B) Schematic representation of replication fork recovery and the recruitment of homologous recombination proteins at the newly synthesized DNA after replication stress (2mM HU); (C) Protein bound to immunoprecipitation (ChIP) with IdU antibody after replication stress; (D) Chromatin associated fractions; (E) Nuclear fraction; (F) Base excision repair proteins recruited at newly synthesized DNA after replication stress in NEIL3 proficient and deficient cells; (G) Replication licensing proteins recruitment in NEIL3 proficient and deficient cells. No statistically significant difference was observed between NEIL3 proficient and deficient cells in data F and G.