Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1.
- Author:
Fan ZHANG
1
;
Zihua GONG
2
Author Information
- Publication Type:Journal Article
- Keywords: DNA double-strand break (DSB); Homologous recombination (HR); Non-homologous end-joining (NHEJ); P53-binding protein 1 (53BP1); Poly(ADP-ribose) polymerase inhibitor (PARPi)
- From: Journal of Zhejiang University. Science. B 2021;22(1):38-46
- CountryChina
- Language:English
- Abstract: Maintenance of cellular homeostasis and genome integrity is a critical responsibility of DNA double-strand break (DSB) signaling. P53-binding protein 1 (53BP1) plays a critical role in coordinating the DSB repair pathway choice and promotes the non-homologous end-joining (NHEJ)-mediated DSB repair pathway that rejoins DSB ends. New insights have been gained into a basic molecular mechanism that is involved in 53BP1 recruitment to the DNA lesion and how 53BP1 then recruits the DNA break-responsive effectors that promote NHEJ-mediated DSB repair while inhibiting homologous recombination (HR) signaling. This review focuses on the up- and downstream pathways of 53BP1 and how 53BP1 promotes NHEJ-mediated DSB repair, which in turn promotes the sensitivity of poly(ADP-ribose) polymerase inhibitor (PARPi) in BRCA1-deficient cancers and consequently provides an avenue for improving cancer therapy strategies.
