RAD51D（也称为RAD51L3）编码蛋白是RAD51重组酶家族的成员，其在同源重组（HR）介导的双链DNA断裂（DSB）中发挥作用。RAD51D与RAD51形成复合物在DSB的早期起作用：切除位于DSB断裂位点侧翼的5'端DNA链和单链突出端被RAD51包被形成核蛋白丝。研究表明，RAD51D与另外三种RAD51旁系同源物形成复合物：XRCC2，RAD51B和RAD51C（称为BCDX2复合物）。该复合物在HR的早期阶段起作用，也是在RAD51募集到受损的DNA处之前。RAD51D还与DNA结合和复制蛋白相互作用，包括SFPQ、NONO、MCM2和MSH2，并且在端粒维持中起作用。RAD51D缺陷的细胞发生自发染色体畸变并表现为G2期停滞。RAD51D的胚系突变会增加卵巢癌和乳腺癌的患病风险。RAD51D体细胞突变在人类癌症中是罕见的，然而，RAD51D变异也与化疗耐药性增加有关。

RAD51D (also known as RAD51L3) is a member of the RAD51 recombinase family that functions in homologous recombination (HR)-mediated repair of double-stranded DNA breaks (DSBs). RAD51D, in complex with RAD51, acts at an early step in the DSB pathway: the 5’ended DNA strands flanking the DSB break site are resected and the single-stranded overhangs are coated by RAD51 forming a nucleo-protein filament. RAD51 then probes for homologous DNA and initiates the process of strand invasion and exchange between homologous DNA. Biochemical studies demonstrate that RAD51D forms a complex with three other RAD51 paralogs: XRCC2, RAD51B and RAD51C (known as the BCDX2 complex). This complex plays a role in the early stages of HR, prior to recruitment of RAD51 to damaged DNA foci. RAD51D also interacts with DNA binding and replication proteins including SFPQ, NONO, MCM2, and MSH2 and has a role in the telomere maintenance. RAD51D-deficient cells develop spontaneous chromosomal aberrations and exhibit G2 arrest. Germline mutations in RAD51D confer increased risk for ovarian cancer and breast cancer. RAD51D somatic mutations are rare in human cancers, however, RAD51D variants have been associated with increased chemoresistance.

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