Figure 7
Figure 7. RA5 and RG2 depend on homology directed repair for radioresistance. Cells were synchronized to the early G1/S border by double thymidine block and were irradiated 1 hour (A) or 5 hours (B) after release into regular medium and assayed for clonogenic survival. (C) Percent knockdown of Rad51 relative to cells infected with control virus after normalization to β-actin. (D-F) Cells were irradiated with indicated doses of γ-IR and assayed for clonogenic survival. Data are mean ± SEM from at least 2 independent experiments. *P < .05, **P < .01, and ***P < .001, for indicated dose relative to HL60 (A-B) or in Rad51-depleted cells relative to “Empty” control cells (D-F).

RA5 and RG2 depend on homology directed repair for radioresistance. Cells were synchronized to the early G1/S border by double thymidine block and were irradiated 1 hour (A) or 5 hours (B) after release into regular medium and assayed for clonogenic survival. (C) Percent knockdown of Rad51 relative to cells infected with control virus after normalization to β-actin. (D-F) Cells were irradiated with indicated doses of γ-IR and assayed for clonogenic survival. Data are mean ± SEM from at least 2 independent experiments. *P < .05, **P < .01, and ***P < .001, for indicated dose relative to HL60 (A-B) or in Rad51-depleted cells relative to “Empty” control cells (D-F).

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