Target intelligence / Profile preview

DNA repair protein RAD51 homolog 2 (RAD51B)

Target
RAD51B
Molecular classification
DNA-binding protein, Enzyme (ATPase), Homologous recombination repair protein, Tumor suppressor complex component, Other (RAD51 paralog)
01

Overview

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].

Other names
RAD51 paralog BRAD51L1REC2R51H2Rad51BhREC2RAD51 homolog BRAD51-like protein 1RecA-like proteinrecombination repair protein
02

Mechanism of action

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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Biological functions

Homologous recombinationDNA double-strand break repairReplication fork protectionGenome stability
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Disease associations

Cancer (including breast, ovarian, and prostate cancer)Fanconi anemia
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Safety considerations

Genomic instability leading to secondary malignanciesHematologic toxicity due to synergistic impairment of DNA repair in normal tissues
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Interacting drugs

PARP inhibitors (e.g., olaparib), as sensitivity to these drugs is enhanced in cells with RAD51B/BCDX2 deficiency[1][5]
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Biomarkers

Mutational status of RAD51B/BCDX2 components for cancer risk and therapy selection[1][5]

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