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. 2010 Nov 10;107(48):20792–20797. doi: 10.1073/pnas.1011412107

Fig. 3.

Fig. 3.

Rev1 suppression inhibits CTX-induced mutagenesis. (A) CTX dose–response curves in control and Rev1-knockdown cells (shRev1-1: P = 0.2555; shRev1-2: P = 0.2209; shRev1-3: P = 0.1062). n = 3 replicates per dose in each sample. P values were determined using an F-test comparison of EC50 values derived from best-fit nonlinear regression curves. (B) A graph showing the relative survival of CTX-treated (4 μg/mL 4-OH-cyclophosphamide for 1 h) control and Rev1-knockdown Eμ-myc lymphoma cells following exposure to 1 μM 6TG for 1 wk. (C) A graph showing the relative survival of CTX-treated (4 μg/mL 4-OH-cyclophosphamide for 1 h) control and Rev1-knockdown L5178Y-TK+/− mouse lymphoma cells following exposure to10 μM triflorothymidine (TFT). (D) A graph showing the relative response of control and Rev1-knockdown Eμ-myc lymphoma cells to multiple rounds of CTX treatment in vitro. In each case lymphoma cell viability was determined 48 h following exposure to 1.3 μg/mL 4-OH-cylophosphamide. Relative drug resistance was determined by normalizing viability measurements to those observed in round 1. P values shown in B–D were determined using Student's t tests.