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. 2023 Mar 11;15(6):1721. doi: 10.3390/cancers15061721

Figure 3.

Figure 3

Involvement of REV7 in double-strand break (DSB) repair. At a DSB lesion, 53BP1–RIF1 recruits the Shieldin complex (SHLD1, SHLD2, SHLD3, and REV7) to block 5’ end resection, and Shieldin also recruits the CST complex (CTC1, STN1, and TEN1) together with DNA polymerase α (Polα) to execute fill-in synthesis, resulting in the inhibition of HR and the facilitation of non-homologous end joining (NHEJ). CHAMP1 binds to REV7 promoting the decreased level of the Shieldin complex, and p31comet–TRIP13 binds to REV7 in the Shieldin complex and promotes its dissociation from SHLD3 by inducing O-REV7 from C-REV7, resulting in a reduction in the Shieldin complex activity.