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. 2022 Mar 1;36(5-6):278–293. doi: 10.1101/gad.349431.122

Figure 4.

Figure 4.

Selective killing of BRCA1/2-deficient cells by different DDR targeted drugs. Both PARPi and REV1i render the ssDNA gaps in BRCA1/2-deficient cells persistent, promoting DSBs or replication catastrophe. POLθi blocks MMEJ and prevents alternative repair of DSBs in HR-defective cells, rendering DSBs persistent in BRCA1/2-deficient cells.