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. Author manuscript; available in PMC: 2019 Jun 17.
Published in final edited form as: Nat Struct Mol Biol. 2018 Oct 29;25(11):1047–1058. doi: 10.1038/s41594-018-0142-5

Figure 2: Selective inhibition of ATR sensitizes SLFN11-deficient cells to CPT treatment.

Figure 2:

a, Efficiency of ATR/ATM knockdown by siRNAs in FG cells was monitored by immunoblotting 5 days after transfection. b, 72 hours after siRNAs transfection, FG cells expressing control or SLFN11 shRNA were treated by 200 nM CPT or DMSO for another 48 hours. Relative cell viabilities were determined by MTS assay. c, d, As in a, b, except with HEK293 cells. e, SLFN11 expression deficiency in MIA PaCa-2 cells was confirmed by immunoblotting. f, g, As in a, b, except with MIA PaCa-2 cells. h, Relative viabilities of FG cells expressing control or SLFN11 shRNA after 48 hours of ATR inhibitor VE-822 and 40 nM CPT treatment were measured by MTS assay. i, Phosphorylation of CHK1 was determined by immunoblotting after 6 hours of 40 nM CPT and VE-822 treatment. j, As in h, except with MIA PaCa-2 cells. k, As in i, with except with MIA Paca-2 cells. Samples were collected after 3 hours treatment. (b, d, g, h, i, biological replicates, mean ± s.d., n = 3). Uncropped images are shown in Supplementary Data Set 1.