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Zihua GONG


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Journal of Zhejiang University SCIENCE B 2021 Vol.22 No.1 P.38-46


Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1

Author(s):  Fan ZHANG, Zihua GONG

Affiliation(s):  Department of Cancer Biology, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44195, USA

Corresponding email(s):   gongz@ccf.org

Key Words:  P53-binding protein 1 (53BP1), DNA double-strand break (DSB), Non-homologous end-joining (NHEJ), Homologous recombination (HR), Poly(ADP-ribose) polymerase inhibitor (PARPi)

Fan ZHANG, Zihua GONG. Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1[J]. Journal of Zhejiang University Science B, 2021, 22(1): 38-46.

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author="Fan ZHANG, Zihua GONG",
journal="Journal of Zhejiang University Science B",
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%0 Journal Article
%T Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1
%A Zihua GONG
%J Journal of Zhejiang University SCIENCE B
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%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.B2000306

T1 - Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1
A1 - Fan ZHANG
A1 - Zihua GONG
J0 - Journal of Zhejiang University Science B
VL - 22
IS - 1
SP - 38
EP - 46
%@ 1673-1581
Y1 - 2021
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.B2000306

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.




Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article


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