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. 2018 Sep 23;20(11):1135–1143. doi: 10.1016/j.neo.2018.08.009

Figure 1.

Figure 1

Verification of synthetic lethality between ATR and PRIM1. (A) Quantification of ATR protein in DLD-1 ATR+/+, ATRs/s, and ATRresc cells by immunoblotting. β-Actin was used as loading control. (B) MMC sensitivity was assessed 120 hours after treatment by proliferation assay in DLD-1 ATR+/+, ATRs/s, and ATRresc cells. (C) Quantification of siRNA-mediated PRIM1 depletion (10 nM) 120 hours after transfection by immunoblotting. β-Actin was used as loading control. (D) Proliferation inhibition was assessed 144 hours after transfection by proliferation assay in DLD-1 ATR+/+, ATRs/s, and ATRresc cells. Error bars represent ±SEM of three independent experiments with each data point reflecting triplicate wells. Asterisks mark statistical significance using a two-tailed, unpaired Student's t test (*P < .05, **P < .01, n.s. = not significant). Immunoblots were performed independently at least twice, and representative results are shown.