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Figure 2. The absence of RANBP9 in NSCLC cells results in increased sensitivity to ATR inhibition. A549 RANBP9 WT controls and A549 RANBP9 KO clones were treated with the ATM inhibitor KU5933 (10 μmol/L; left panel) and the ATR inhibitor VE-821 (10 μmol/L; right panel). Growth was monitored automatically by live cell imaging (Incuyte^TM) and cell confluence was quantitated in three replica plates. RANBP9: RAN binding protein 9; NSCLC: non-small cell lung cancer; ATR: ataxia and telangiectasia-related; KO: knockout; ATM: ataxia telangiectasia mutated