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. 2011 Feb 7;108(8):3406–3411. doi: 10.1073/pnas.1013715108

Fig. 6.

Fig. 6.

NHEJ contributes to PARP inhibitor-induced effects in other HR-deficient contexts. (A) BRCA1-deficient HCC1937 and BRCA1-reconstituted HCC1937/BRCA1 cells were continuously exposed to ABT-888 in the presence or absence of 125 nM DNA-PK inhibitor (DNA-PKi) and assayed for clonogenic survival. (Inset) Western blots of cell lysates from HCC1937 and HCC1937/BRCA1. (B) Western blots of M059J and reconstituted M059J?PKcs lines showing the restoration of DNA-PKcs expression and the shRNA-mediated knockdown of BRCA1. (C) Clonogenic survival of shRNA–transfected M059J/M059J?PKcs lines treated with ABT-888 for 72 h. (D) Clonogenic survival of ATM-deficient GM16666 or ATM-reconstituted GM16667 fibroblasts. Cells were exposed to ABT-888 for 48 h in the presence or absence of 250 nM DNA-PK inhibitor (DNA-PKi), washed, and allowed to form colonies. (Inset) Western blots of lysates from GM16666 and GM16667 fibroblasts. Data are displayed as mean ± SEM of triplicate plates. Results are representative of three independent experiments.