Unrepairable DNA double-strand breaks that are generated by ionising radiation determine the fate of normal human cells

2012 ◽  
Vol 125 (22) ◽  
pp. 5280-5287 ◽  
Author(s):  
Asao Noda ◽  
Yuko Hirai ◽  
Kanya Hamasaki ◽  
Hiroshi Mitani ◽  
Nori Nakamura ◽  
...  
1998 ◽  
Vol 149 (5) ◽  
pp. 440 ◽  
Author(s):  
Ryuichi Okayasu ◽  
Katsutoshi Suetomi ◽  
Robert L. Ullrich

1989 ◽  
Vol 219 (2) ◽  
pp. 95-100 ◽  
Author(s):  
Peter J. Mayer ◽  
Christopher S. Lange ◽  
Matthews O. Bradley ◽  
Warren W. Nichols

2005 ◽  
Vol 164 (4) ◽  
pp. 514-517 ◽  
Author(s):  
Francesca Antonelli ◽  
Mauro Belli ◽  
Giacomo Cuttone ◽  
Valentina Dini ◽  
Giuseppe Esposito ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Lei Zhao ◽  
Chengyu Bao ◽  
Yuxuan Shang ◽  
Xinye He ◽  
Chiyuan Ma ◽  
...  

Ionising radiation- (IR-) induced DNA double-strand breaks (DSBs) are considered to be the deleterious DNA lesions that pose a serious threat to genomic stability. The major DNA repair pathways, including classical nonhomologous end joining, homologous recombination, single-strand annealing, and alternative end joining, play critical roles in countering and eliciting IR-induced DSBs to ensure genome integrity. If the IR-induced DNA DSBs are not repaired correctly, the residual or incorrectly repaired DSBs can result in genomic instability that is associated with certain human diseases. Although many efforts have been made in investigating the major mechanisms of IR-induced DNA DSB repair, it is still unclear what determines the choices of IR-induced DNA DSB repair pathways. In this review, we discuss how the mechanisms of IR-induced DSB repair pathway choices can operate in irradiated cells. We first briefly describe the main mechanisms of the major DNA DSB repair pathways and the related key repair proteins. Based on our understanding of the characteristics of IR-induced DNA DSBs and the regulatory mechanisms of DSB repair pathways in irradiated cells and recent advances in this field, We then highlight the main factors and associated challenges to determine the IR-induced DSB repair pathway choices. We conclude that the type and distribution of IR-induced DSBs, chromatin state, DNA-end structure, and DNA-end resection are the main determinants of the choice of the IR-induced DNA DSB repair pathway.


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