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Defects in double-strand break response are restored by preventing Skp2-dependent ubiquitination of Nbs1 in RecQL4-defective cells.A, ubiquitination of wildtype (WT) or K735R Nbs1 (735) in mock- or RecQL4-depleted 293T cells treated with neocarzinostatin. B, percentages of Mre11 and Rad51 foci-positive cells, 1 h after neocarzinostatin treatment in cells expressing wildtype (WT) or K735R (735) Nbs1. ∗∗∗p < 0.001; ns, not significant.
