Promyelocytic leukemia protein interacts with werner syndrome helicase and regulates double-strand break repair in γ-irradiation-induced DNA damage responses

2011 ◽  
Vol 76 (5) ◽  
pp. 550-554 ◽  
Author(s):  
Jilai Liu ◽  
Yi Song ◽  
Junjie Qian ◽  
Bin Liu ◽  
Yan Dong ◽  
...  
Keyword(s):  
Dna Damage ◽  
Werner Syndrome ◽  
Strand Break ◽  
Double Strand Break ◽  
Promyelocytic Leukemia ◽  
Double Strand Break Repair ◽  
Γ Irradiation ◽  
Promyelocytic Leukemia Protein ◽  
Dna Damage Responses ◽  
Break Repair

scholarly journals DNA Damage Responses: Beyond Double-Strand Break Repair

2015 ◽  
Vol 25 (1) ◽  
pp. R45-R46 ◽  
Author(s):  
Andrea L. Bredemeyer ◽  
Barry P. Sleckman
Keyword(s):  
Dna Damage ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dna Damage Responses ◽  
Break Repair

scholarly journals The nucleoporin 153, a novel factor in double-strand break repair and DNA damage response

Oncogene ◽  
2012 ◽  
Vol 31 (45) ◽  
pp. 4803-4809 ◽  
Author(s):  
C Lemaître ◽  
B Fischer ◽  
A Kalousi ◽  
A-S Hoffbeck ◽  
J Guirouilh-Barbat ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Damage Response ◽  
Break Repair

scholarly journals Involvement of POLA2 in Double Strand Break Repair and Genotoxic Stress

2020 ◽  
Vol 21 (12) ◽  
pp. 4245
Author(s):  
Tuyen T. Dang ◽  
Julio C. Morales
Keyword(s):  
Dna Damage ◽  
Genomic Instability ◽  
Dna Polymerase ◽  
Genotoxic Stress ◽  
Strand Break ◽  
Double Strand Break ◽  
Double Strand Break Repair ◽  
Dsb Repair ◽  
Dna Polymerase Alpha ◽  
Break Repair

Cellular survival is dependent on the efficient replication and transmission of genomic information. DNA damage can be introduced into the genome by several different methods, one being the act of DNA replication. Replication is a potent source of DNA damage and genomic instability, especially through the formation of DNA double strand breaks (DSBs). DNA polymerase alpha is responsible for replication initiation. One subunit of the DNA polymerase alpha replication machinery is POLA2. Given the connection between replication and genomic instability, we decided to examine the role of POLA2 in DSB repair, as little is known about this topic. We found that loss of POLA2 leads to an increase in spontaneous DSB formation. Loss of POLA2 also slows DSB repair kinetics after treatment with etoposide and inhibits both of the major double strand break repair pathways: non-homologous end-joining and homologous recombination. In addition, loss of POLA2 leads to increased sensitivity to ionizing radiation and PARP1 inhibition. Lastly, POLA2 expression is elevated in glioblastoma multiforme tumors and correlates with poor overall patient survival. These data demonstrate a role for POLA2 in DSB repair and resistance to genotoxic stress.

scholarly journals PARP1-dependent recruitment of KDM4D histone demethylase to DNA damage sites promotes double-strand break repair

2014 ◽  
Vol 111 (7) ◽  
pp. E728-E737 ◽  
Author(s):  
H. Khoury-Haddad ◽  
N. Guttmann-Raviv ◽  
I. Ipenberg ◽  
D. Huggins ◽  
A. D. Jeyasekharan ◽  
...  
Keyword(s):  
Dna Damage ◽  
Strand Break ◽  
Double Strand Break ◽  
Histone Demethylase ◽  
Double Strand Break Repair ◽  
Break Repair
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