Fig. 1
From: PARP inhibitor resistance: the underlying mechanisms and clinical implications
Schematic describing the function the principle of synthetic lethality interaction between PARPs and BRCA1/2. When cells suffer from DNA response, single-strand breaks emerge. PARPs, especially PARP1, bind to the DNA break sites, which result in the PARylation of target proteins and recrement of the DNA damage repair effectors. Then the auto-PARylation on PARPs leads to the dissociation of PARPs from DNA. Treating HR-deficient tumor cells with PARPi, NHEJ is the only pathway to use to repair double-strand break, which lead to accumulation of genome instability and cell death for the low fidelity