USP11 silencing impairs HR repair at double-strand breaks. A, RAD51 foci were scored by immunofluorescent imaging at the indicated times after treatment with IR (*, p = 0.001; **, p = 0.038). B, mock, non-targeting and USP11-silenced cells were plated in 60-mm dishes and treated with the indicated doses of IR. Colonies of >50 cells were scored 7–10 days after irradiation. Error bars represent S.D. (n = 3). C–E, non-targeting, BRCA1- and USP11-silenced U2OS cells were treated with C, bleomycin (1 μg/ml), D, cisplatin (5 μm), or E, mitomycin C (0.2 μg/ml) for 96 h followed by measurement of viability (*, p < 0.05). Error bars are S.D. (n = 4). F, non-targeting, BRCA1- and USP11-silenced HEK293 cells containing an integrated HR repair substrate were transfected with I-SceI to induce a double-strand break in the reporter gene. The percentage of GFP+ cells was scored by flow cytometry. (Error bars are S.D., n = 3, *, p = 0.046). G, USP11 and BRCA1 protein levels in the cells used in F were measured by immunoblotting.