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This recruitment is central not only for assembling DNA repair proteins and modulating ATM‐dependent checkpoint signaling but also for organizing nuclear repair compartments that protect vulnerable genomic loci."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its initial recruitment, TP53BP1 is a master regulator of double‐strand break repair pathway choice. It functions to limit DNA-end resection, thereby promoting non-homologous end joining (NHEJ) over homologous recombination, often through antagonism of BRCA1 activity. Its interplay with effector proteins such as RIF1 and the newly identified shieldin complex enforces a nucleosomal barrier that protects DNA ends, while post-translational modifications including acetylation and phosphorylation modulate its binding affinity and release from chromatin. In this way, TP53BP1 integrates histone modification cues with repair protein recruitment to steer repair outcomes in a cell cycle–dependent manner."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its direct role in the repair process, TP53BP1 plays critical functions in checkpoint activation and genome integrity maintenance. By interfacing with p53 and associated regulators such as USP28, it amplifies stress-responsive gene transactivation and enforces cell cycle arrest following DNA insult. Its dynamic regulation—for example, by mitosis-specific phosphorylation events that temporarily prevent chromatin binding and by dephosphorylation events that permit DDR restoration in G1—underscores its multifaceted roles in coordinating timely repair, preserving chromatin structure, and influencing therapeutic outcomes in cancer. 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