RAD51B（也称为RAD51L1）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（DSBs）中发挥作用。RAD51B 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。RAD51B表达在接受电离辐射后上调并且RAD51B是形成修复复合物必须的，包括RAD51旁系同源基因, XRCC2和XRCC3。除了DNA损伤修复途径外，RAD51B还通过对p53、CDK2和细胞周期蛋白E的磷酸化来影响细胞周期调控，导致G1细胞周期延迟。RAD51B胚系变异与家族性乳腺癌和胶质母细胞瘤的发生风险有关。RAD51表达缺失导致DNA修复功能丧失，并可能通过基因组不稳定性促进肿瘤发生。

RAD51B (also known as RAD51L1) is a member of the RAD51 recombinase family that functions in homologous recombination (HR)-mediated repair of double-stranded DNA breaks (DSBs). RAD51B, in complex with the central homologous repair protein 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. RAD51B expression is upregulated following ionizing radiation and RAD51B function is required for the formation of repair complexes including RAD51 paralogs, XRCC2 and XRCC3. In addition to the DNA damage repair pathway, RAD51B has been shown to influence cell cycle regulation through phosphorylation of p53, CDK2 and cyclin E, resulting in G1 cell cycle delay. Germline RAD51B variants have been identified as risk factors in familial breast cancer and glioblastoma. Loss of RAD51B expression results in loss of DNA repair functions and may promote oncogenesis via genome instability.

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