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DNA repair protein RAD51 homolog 2 (RAD51B) is one of five human RAD51 paralogs and functions as a key component of the BCDX2 complex (RAD51B–RAD51C–RAD51D–XRCC2), which plays a critical role in homologous recombination—a major pathway for repairing DNA double-strand breaks and maintaining genome integrity[1][2][3][5]. RAD51B is an ATPase that, together with other paralogs, stabilizes and promotes the assembly of RAD51 filaments on single-stranded DNA at damage sites, facilitating DNA repair during replication and after DNA-damaging insults[1][2][4][5]. Mutations in RAD51B cause defects in DNA repair, increased genomic instability, and predisposition to cancers such as breast, ovarian, and prostate cancer, and can lead to Fanconi anemia when combined with other DNA repair deficiencies[1][5]. RAD51B is not a receptor but an enzyme and DNA-binding component essential for tumor suppression and genome maintenance. Cells with loss of RAD51B function are hypersensitive to PARP inhibitors, making RAD51B and its complex a clinically relevant cancer vulnerability and potential biomarker for therapy with DNA repair-targeted agents[1][5].
Synthetic lethality via inhibition of parallel DNA repair mechanisms (e.g., PARP inhibition increases cell death in RAD51B-deficient cells)[1][5]
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