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. 2013 Jun 24;110(28):11415–11420. doi: 10.1073/pnas.1301672110

Fig. 5.

Fig. 5.

NS binds RAD51 and promotes its recruitment to DNA damage foci. (A) Overexpression of RAD51, but not that of BRCA2 or RPA70, rescues the γ-H2AX+ cell percentage of NSKO MEF cells. (B) CoIP of endogenous NS and RAD51 by anti-RAD51 (left) or anti-NS antibody (right) confirms that these two proteins interact with each other in vivo. (C) HU treatment increases the percentages of γ-H2AX+ in both siScr- and siNS-treated MEF cells. siNS-treated cells show more DNA damage events than siScr-treated cells. (D) The HU effect on triggering RAD51+ foci in siNS-treated MEF cells is significantly reduced compared that in siScr-treated cells. (Scale bar: 50 µm.) (E) DSB-ChIP assays show that the physical recruitment of RAD51 to I-SceI–induced DSBs is significantly attenuated by NSKD (siNS) at the 24 and 48-h time points following the induction of I-SceI expression.