DNA double-strand breaks can be generated by exposure to ionizing radiation or through endogenous cellular reactions. Double-strand breaks are generally thought to be repaired via one of two distinct mechanisms: homologous recombination (HR) or non-homologous end joining (NHEJ). Homologous recombination requires the activity of the members of the RAD52 epistasis group, which includeRAD50, RAD51, RAD52, RAD54, RDH54/TID1, RAD55, RAD57, RAD59, MRE11, and XRS2. RAD52 can catalyze strand annealing reactions, and can form oligomers that attach to ends of single-stranded DNA.
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Protein Aliases: DNA repair protein RAD52 homolog; recombination protein RAD52; rhabdomyosarcoma antigen MU-RMS-40.23
Gene Aliases: RAD52; Rad52yh