Figure 6.

PARP1-dependent end-joining is hindered by the presence of Ku but not modulated by DNA-PKcs. Cells were treated with either DIQ (75 µM) or the DNA-PK-inhibitor NU7026 (15 µM) or with both inhibitors simultaneously. (A) I-SceI was used to linearize pEJ plasmid in vitro of which 1.6 µg were then transfected using lipofectamine 2000 (Invitrogen, Germany) into DNA-PK-deficient (V3) and proficient (AA8) hamster cells. The % GFP⁺ cells were measured as an indicator of the repair after 24 and 48 h with or without DIQ. (B) Experiments were performed as described in Figure 4C. Inhibition of DNA-PKcs but not of PARP compromised the repair in CHOK1. (C) Inhibition of PARP but not of DNA-PK almost completely inhibited the slow repair in xrs5 cells.