Abstract

This review focuses on DNA–dependent protein kinase (DNA–PK), which is the key regulator of canonical non–homologous end–joining (NHEJ), the predominant mechanism of DNA double–strand break (DSB) repair in mammals. DNA–PK consists of the DNA–binding Ku70/80 heterodimer and the catalytic subunit DNA–PKcs. They assemble at DNA ends, forming the active DNA–PK complex, which initiates NHEJ–mediated DSB repair. Paradoxically, both Ku and DNA–PKcs are associated with telomeres, and they play crucial roles in protecting the telomere against fusions. Herein, we discuss possible mechanisms and contributions of Ku and DNA–PKcs in telomere regulation.

Details

Title
DNA–dependent protein kinase in telomere maintenance and protection
Author
Sui, Jiangdong 1   VIAFID ORCID Logo  ; Zhang, Shichuan 2 ; Chen, Benjamin P. C. 3 

1  Chongqing University Cancer Hospital, Radiation Oncology Center, Chongqing, China (GRID:grid.190737.b) (ISNI:0000 0001 0154 0904) 
2  Sichuan Cancer Hospital, Department of Radiation Oncology, Chengdu, China (GRID:grid.415880.0) (ISNI:0000 0004 1755 2258) 
3  University of Texas Southwestern Medical Center, Department of Radiation Oncology, Dallas, USA (GRID:grid.267313.2) (ISNI:0000 0000 9482 7121) 
Pages
2
Publication year
2020
Publication date
Dec 2020
Publisher
Springer Nature B.V.
ISSN
1425-8153
e-ISSN
1689-1392
Source type
Scholarly Journal
Language of publication
English
DOI
https://doi.org/10.1186/s11658-020-0199-0
ProQuest document ID
2788426683
Copyright
© The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.