The hMre11-hRad50-NBS1 protein plays a central role in the human cellular DNA-Damage response, with recent studies indicating that these proteins help link DNA-damage detection to DNA-repair and cell cycle-checkpoint functions. This protein complex has been implicated in the activation of cell cycle-regulatory pathways, due to the fact that the NBS1 gene mutates in the chromosomal-instability syndrome, Nijmegen breakdown syndrome (NBS), which is characterized by increased cancer incidence, cell cycle checkpoint defects, and ionizing radiation sensitivity. HMre11-hRad50 foci form in response to DNA double-strand breaks and rely upon a DNA damage-induced signaling pathway. However, hMre11 migrates to sites of damage while hRad51 does not localize at these sites. These findings are consistent with the distinct role of these proteins in DNA repair.

MRE11 antibodies are useful tools for DNA repair research, cell cycle research, and for certian cancer studies.