DNA double-strand breaks (DSBs) are generated during intrinsic eukaryotic DNA recombination events such as assembly of antigen receptor genes, meiotic and miotic recombination. DNA DSB repair proteins are also required to repair breaks induced by extrinsic factors such as ionizing radiation and mutagenic chemicals. Originally identified in S. cerevisiae, Rad50 is one of a group of genes, designated as the Rad52 epistasis group, whose products mediate DSB repair. Many of these genes, including Rad50, are conserved in humans and are thought to have a similar function to their S. cerevisiae counterparts. In yeast, a multiprotein complex of Rad50, MRE11, and XRS2 has been implicated in the nucleocytic processing of DSBs. In humans, Rad50 and MRE11 complex with up to three additional proteins (95 kDa, 200 kDa, and 350 kDa). The 95 kDa species is thought to be human XRS2, although a separate report has identified it as Nibrin, the product of the gene mutated in Nijmegen breakage syndrome. The Rad50-MRE11-p95 complex possess endonuclease and 3' to 5' exonuclease activity. Thus, human Rad50 functions in a multiprotein complex to mediate the repair of DSBs in the human genome.
This antibody is routinely tested by western blot analysis. Other applications were tested at BD Biosciences Pharmingen during antibody development only or reported literature.