DNA repair protein RAD52 homolog (RAD52)

DNA repair protein RAD52 homolog (RAD52) is a conserved DNA repair factor central to the maintenance of genome integrity. RAD52 facilitates the annealing of complementary single-stranded DNA during repair of double-strand breaks by single-strand annealing and serves as a backup mediator for homologous recombination, especially in cells deficient in canonical HR proteins such as BRCA1/2 or PALB2[1][2][5]. Structurally, RAD52 forms heptameric or undecameric rings via its N-terminal domain, mediating DNA binding and annealing, while its intrinsically disordered C-terminal tail participates in protein-protein interactions[2][6]. In mammals, RAD52 plays key roles in alternative DNA repair pathways, RNA-templated DNA recombination, break-induced replication, and regulation of replication fork stability[1][3][5][6]. RAD52 is considered a promising therapeutic target, particularly in cancer cells with impaired HR, where its inhibition can induce synthetic lethality[3][1][2]. RAD52 overexpression is linked to tumorigenesis, and targeting RAD52 is a strategy under investigation for the selective eradication of DNA repair-deficient cancers[3][1].

Other names

RAD52DNA repair protein RAD52 homologRadiation sensitive 52Recombination protein RAD52RAD52 homologRhabdomyosarcoma antigen MU-RMS-40.23

Inhibiting DNA double-strand break repair via SSA and backup HR pathways; Synthetic lethality with BRCA1/2, PALB2, and other HR-deficient tumor cells; Protects replication fork and promotes survival in DNA repair-deficient cancers