hMre11 and hRad50 nuclear foci are induced during the normal cellular response to DNA double-strand breaks.

摘要: We previously identified a conserved multiprotein complex that includes hMre11 and hRad50. In this study, we used immunofluorescence to investigate the role of in DNA double-strand break (DSB) repair. hRad50 form discrete nuclear foci response treatment with DSB-inducing agents but not UV irradiation. colocalize after ionizing radiation are distinct from those DSB repair protein, hRad51. Our data indicate an irradiated cell is competent either hMre11-hRad50 or hRad51 foci, both. The multiplicity much higher repair-deficient line 180BR than repair-proficient cells. focus formation markedly reduced cells derived ataxia-telangiectasia patients, whereas increased. These experiments support genetic evidence Saccharomyces cerevisiae indicating Mre11-Rad50 have roles Rad51 Further, these DSBs dependent upon damage-induced signaling pathway.