Eukaryotic organisms constantly face a wide range of internal and external factors that cause damage to their DNA. Failure to accurately and efficiently repair these DNA lesions can result in genomic instability and the development of tumors (Canela et al., 2017). Among the various forms of DNA damage, DNA double-strand breaks (DSBs) are particularly harmful. Two major pathways, non-homologous end joining (NHEJ) and homologous recombination (HR), are primarily responsible for repairing DSBs (Katsuki et al., 2020; Li and Yuan, 2021; Zhang and Gong, 2021; Xiang et al., 2023). NHEJ is an error-prone repair mechanism that simply joins the broken ends together (Blunt et al., 1995; Hartley et al., 1995). In contrast, HR is a precise repair process. It involves multiple proteins in eukaryotic cells, with the RAD51 recombinase being the key player, which is analogous to bacterial recombinase A (RecA) (Shinohara et al., 1992). The central event in HR is the formation of RAD51-single-stranded DNA (ssDNA) nucleoprotein filaments that facilitate homology search and DNA strand invasion, ultimately leading to the initiation of repair synthesis (Miné et al., 2007; Hilario et al., 2009; Ma et al., 2017).
同源重组（HR）是一种高度精确的DNA双链断裂（DSB）损伤修复方式。HR修复的关键步骤是重组酶RAD51通过包裹单链DNA形成核酸蛋白纤维丝，进行同源模板搜索，并进行DNA链入侵反应，从而启动DNA修复合成。本研究发现，纤维蛋白（FBL）是重要的HR调节因子。一旦发生DNA损伤，FBL就被招募到DSB位点，并直接与RAD51互作。细胞缺失FBL会导致RAD51在DNA损伤位点募集减少，HR修复效率降低。此外，细胞缺失FBL会导致染色体畸变增加，促使细胞对DNA损伤药物敏感。本研究提出了FBL介导的RAD51在DNA损伤位点的招募的新机制，并强调了FBL在癌症治疗中的潜在意义。.
同源重组（HR）是一种高度精确的DNA双链断裂（DSB）损伤修复方式。HR修复的关键步骤是重组酶RAD51通过包裹单链DNA形成核酸蛋白纤维丝，进行同源模板搜索，并进行DNA链入侵反应，从而启动DNA修复合成。本研究发现，纤维蛋白（FBL）是重要的HR调节因子。一旦发生DNA损伤，FBL就被招募到DSB位点，并直接与RAD51互作。细胞缺失FBL会导致RAD51在DNA损伤位点募集减少，HR修复效率降低。此外，细胞缺失FBL会导致染色体畸变增加，促使细胞对DNA损伤药物敏感。本研究提出了FBL介导的RAD51在DNA损伤位点的招募的新机制，并强调了FBL在癌症治疗中的潜在意义。