Science Advances

Supplementary Materials

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  • Fig. S1. Loss of PARG impairs DNA damage repair.
  • Fig. S2. Kinetics of γ-H2AX foci formation in the PARG knockdown cells.
  • Fig. S3. Identification of novel PARG inhibitors.
  • Fig. S4. COH34 prolongs PARylation in cells.
  • Fig. S5. SDS-PAGE and Coomassie blue staining analysis of PARG catalytic domain.
  • Fig. S6. COH34 traps DNA damage repair factors for a prolonged time.
  • Fig. S7. COH34 treatment impairs DNA damage repair.
  • Fig. S8. COH34 treatment impairs HR, c-NHEJ, and a-NHEJ pathways.
  • Fig. S9. COH34 targets the catalytic site of PARG in cells.
  • Fig. S10. COH34 treatment induces γ-H2AX foci formation and increases the level of PARylation in BRCA-mutant and PARP inhibitor–resistant cancer cells.
  • Fig. S11. Efficacy of olaparib in TNBC cell lines.
  • Fig. S12. COH34 treatment selectively suppresses BRCA-deficient tumor cell growth.
  • Fig. S13. HCC1395 and HCC1937 cancer cells are more sensitive to COH34 treatment compared to olaparib treatment.
  • Fig. S14. Half-life of COH34 in mice.
  • Fig. S15. COH34 induces apoptosis of DNA repair–defective NSCLC.
  • Fig. S16. COH34 treatment increases PARylation level in S phase cells.

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