Target intelligence / Profile preview

DNA repair protein RAD51 homolog C (RAD51C)

Target
RAD51C
Molecular classification
DNA repair protein, RAD51 paralog, Other
01

Overview

DNA repair protein RAD51 homolog C (RAD51C) is a key component of the homologous recombination DNA repair pathway, acting as a central member of two major protein complexes: BCDX2 (RAD51B-RAD51C-RAD51D-XRCC2) and CX3 (RAD51C-XRCC3)[1][3][5]. RAD51C orchestrates RAD51 filament assembly on single-stranded DNA, promoting the accurate repair of double-strand breaks and protecting replication forks[3]. The protein is essential for genome stability and viability—mutations in RAD51C predispose to several cancers, particularly breast and ovarian cancer, and can underlie Fanconi anemia group O (FANCO)[1][3][5]. RAD51C functions as both an early mediator (regulating RAD51 loading) and a late actor (participating in Holliday junction resolution) during HR-mediated DNA repair. Loss or dysfunction leads to sensitivity to DNA-damaging agents and synthetic lethality with PARP inhibition, making RAD51C-deficient cancers susceptible to agents such as olaparib[3]. RAD51C is not a classic receptor, enzyme, or transporter—it is classified as a DNA repair protein and is often considered in the context of cancer therapy for its biomarker and synthetic lethality roles.

Other names
RAD51L2FANCORAD51 homolog CRAD51-like protein 2BROVCA3R51H3yeast RAD51 homolog 3
02

Mechanism of action

Inhibitors such as PARP inhibitors exploit synthetic lethality in cancer cells deficient in RAD51C-mediated homologous recombination repair, leading to cell death

03

Biological functions

Homologous recombinationDNA double-strand break repairReplication fork protection and restartMaintenance of genome stabilityMeiotic and mitotic DNA repair
04

Disease associations

Cancer (including breast, ovarian, and prostate cancer)Fanconi anemia (FANCO group)Genome instability disorders
05

Safety considerations

Risk of genome instability and tumorigenesis with loss-of-function variantsPotential for toxicity in normal proliferating tissues when targeted indirectly with DNA-damaging agents or PARP inhibitors
06

Interacting drugs

Olaparib (and other PARP inhibitors, through synthetic lethality in HR-deficient tumors; indirect interaction)
07

Biomarkers

RAD51C mutation status as a biomarker for HR deficiencyRAD51C protein expression/foci as an indicator of HR activity

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