{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nXRCC1 is a pivotal, non‐enzymatic scaffold protein that orchestrates DNA repair by assembling multiprotein complexes required for both base excision repair (BER) and single‐strand break repair (SSBR). Mechanistic studies demonstrate that XRCC1 is rapidly recruited to sites of DNA damage—often via poly(ADP‐ribose) signals generated by PARP enzymes—and facilitates repair by bridging enzymes such as DNA ligase III, APE1, polynucleotide kinase/phosphatase, and the glycosylase hOGG1. Through these interactions, XRCC1 promotes the efficient processing of oxidized and alkylated bases and maintains genomic stability by channeling repair intermediates to downstream enzymes that complete strand resealing."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurther investigations have elucidated that XRCC1 not only provides a physical platform for a host of repair enzymes but also co‐localizes with replication factors such as PCNA during S phase, thereby synchronizing repair with DNA synthesis. Its interactions enhance the catalytic activities of partner proteins (for example, stimulating hOGG1 glycosylase activity) and promote the hand‐off of repair intermediates between enzymes. This coordination minimizes the persistence of DNA breaks that could otherwise trigger genomic instability."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nEpidemiologic and clinical studies have explored how genetic variations in XRCC1—particularly non‐synonymous polymorphisms such as Arg399Gln, Arg194Trp, and Arg280His—modulate DNA repair capacity and influence cancer susceptibility and therapeutic responses. Many investigations across diverse tumor types (including lung, breast, bladder, gastric, esophageal, and ovarian cancers) indicate that altered XRCC1 function, as manifested by these variants, correlates with increased DNA adduct levels, mutagen sensitivity, and differential outcomes following chemotherapy or radiotherapy. This body of work underscores the clinical relevance of XRCC1 as both a biomarker of repair proficiency and a potential mediator of individual risk in carcinogenesis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}, {"type": "fg_fs", "start_ref": "9", "end_ref": "11"}, {"type": "fg_f", "ref": "21"}, {"type": "fg_fs", "start_ref": "12", "end_ref": "14"}, {"type": "fg_fs", "start_ref": "22", "end_ref": "24"}, {"type": "fg_f", "ref": "18"}, {"type": "fg_f", "ref": "25"}, {"type": "fg_f", "ref": "3"}, {"type": "fg_f", "ref": "27"}, {"type": "fg_f", "ref": "17"}, {"type": "fg_fs", "start_ref": "29", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditionally, several studies have emphasized that perturbations in XRCC1 function—whether through direct genetic mutations or single‐nucleotide polymorphisms—can lead to compromised DNA repair efficiency, resulting in increased cellular sensitivity to DNA‐damaging agents and contributing to genomic instability. These findings not only solidify the essential role of XRCC1 in preserving DNA integrity but also highlight its potential as a therapeutic target; for instance, defective XRCC1 function has been linked to adverse outcomes in neurodegenerative disorders and may be modulated to improve responses to cancer therapies."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "8"}, {"type": "fg_f", "ref": "42"}, {"type": "fg_f", "ref": "21"}, {"type": "fg_f", "ref": "2"}, {"type": "fg_f", "ref": "23"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, the studies across diverse model systems and patient populations underscore that XRCC1 is not only fundamental for mediating prompt and efficient repair of endogenous and exogenous DNA single‐strand breaks but also plays a critical role in modulating individual susceptibility to cancer and treatment response. Ongoing research into XRCC1’s mechanistic interactions and the impact of its genetic variants will continue to provide insights into its contribution to genomic maintenance and its value as a biomarker and potential therapeutic target in precision medicine."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}, {"type": "fg_f", "ref": "8"}, {"type": "fg_f", "ref": "20"}, {"type": "fg_fs", "start_ref": "9", "end_ref": "11"}, {"type": "fg_f", "ref": "1"}, {"type": "fg_f", "ref": "42"}, {"type": "fg_f", "ref": "21"}, {"type": "fg_fs", "start_ref": "12", "end_ref": "14"}, {"type": "fg_f", "ref": "2"}, {"type": "fg_fs", "start_ref": "22", "end_ref": "24"}, {"type": "fg_f", "ref": "18"}, {"type": "fg_f", "ref": "25"}, {"type": "fg_f", "ref": "3"}, {"type": "fg_f", "ref": "27"}, {"type": "fg_f", "ref": "17"}, {"type": "fg_f", "ref": "29"}, {"type": "fg_f", "ref": "4"}, {"type": "fg_f", "ref": "31"}, {"type": "fg_f", "ref": "5"}, {"type": "fg_f", "ref": "32"}, {"type": "fg_f", "ref": "15"}, {"type": "fg_fs", "start_ref": "33", "end_ref": "41"}, {"type": "fg_f", "ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jae Yong Park, Su Yeon Lee, Hyo-Sung Jeon, et al. 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