Fig. 2: Loss of KLF5 hypersensitizes cells to replication stress.
From: KLF5 loss sensitizes cells to ATR inhibition and is synthetic lethal with ARID1A deficiency
a Western blot analysis of KLF5 protein levels in U2-OS cells following CRISPR-mediated gene knockout (KO). GAPDH was used as loading control. Representative of at least 5 independent experiments. b, c Clonogenic survivals of WT and KLF5 KO U2-OS (b), and RPE-1 (c) cells treated with ATRi. d alamarBlue cell viability assay of WT and KLF5 KO HAP-1 cells upon treatment with ATRi, (biological n = 3). e Clonogenic survivals of WT and KLF5 KO U2-OS cells, complemented with GFP-only or with WT KLF5-GFP, treated with ATRi (AZD6738). f–h Clonogenic survivals of WT and KLF5 KO U2-OS cells treated with CHK1i (e), hydroxyurea (f), or camptothecin (g). Error bars represent means ± SEM from at least three biologically independent experiments. Data represented as AUCs (area under the curves). Statistical analyses were performed using a one-way ANOVA test with multiple comparisons. ns not significant. Source data are provided as a Source Data file.
