{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRECQL, the most abundant member of the human RecQ family of helicases, plays a crucial role in safeguarding genome integrity by promoting the restart of stalled replication forks and ensuring proper replication origin firing. Studies have demonstrated that RECQL facilitates the rapid restoration of fork progression after topoisomerase I inhibition and is recruited to replication origins in a cell cycle–dependent manner, highlighting its importance in DNA replication dynamics and in preventing the formation of harmful double‐strand breaks."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBiochemical investigations have revealed that RECQL exhibits robust ATP‐dependent DNA helicase activity along with strand annealing and branch migration functions. Its substrate specificity is distinct from other RecQ helicases—for instance, RECQL does not unwind certain noncanonical structures like G-quadruplexes but efficiently disrupts specific Holliday junction and DNA fork structures. Structural studies have identified critical domains, such as the N-terminal region and a prominent β-hairpin within the winged-helix domain, which govern oligomerization and dictate the switch between DNA unwinding and strand annealing. These properties, together with its regulated formation of higher-order oligomers, underscore the dual and dynamic enzymatic functions of RECQL."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "12"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its core helicase activity, RECQL integrates multiple DNA repair pathways through direct interactions with key genome surveillance factors such as replication protein A, PARP1, and Ku70/80. It contributes to homologous recombination, base excision repair (including a novel long-patch sub-pathway), and nonhomologous end-joining, while additionally participating in the processing of Holliday junctions and in telomere maintenance. Importantly, the functional impairment or mutation of RECQL has been linked to genomic instability and cancer predisposition—most notably in familial breast cancer—as well as to therapeutic vulnerabilities in diverse tumor types. These clinical correlations, together with reports of deleterious RECQL alleles causing genome instability syndromes and altering responses to replication stress and chemotherapeutic agents, emphasize the pivotal role of RECQL in cellular DNA metabolism and its potential as a prognostic marker and therapeutic target. Recent evidence even hints at a role for RECQL in modulating viral replication dynamics."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "13", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Matteo Berti, Arnab Ray Chaudhuri, Saravanabhavan Thangavel, et al. 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