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