scholarly journals Enhancing sensitization of S-phase cells to high-linear energy transfer radiation by inhibition of homologous recombination repair

Cell Cycle ◽  
2009 ◽  
Vol 8 (9) ◽  
pp. 1451-1452 ◽  
Author(s):  
Hongyan Wang ◽  
Ya Wang
2009 ◽  
Vol 74 (4) ◽  
pp. 1236-1241 ◽  
Author(s):  
Hongyan Wang ◽  
Shuang Liu ◽  
Piyan Zhang ◽  
Shimeng Zhang ◽  
Mamta Naidu ◽  
...  

2007 ◽  
Vol 254 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Sami Benzina ◽  
Frederic Debomy ◽  
Jean-Pierre Bergerat ◽  
Jean-Marc Denis ◽  
John Gueulette ◽  
...  

2007 ◽  
Vol 18 (10) ◽  
pp. 4062-4073 ◽  
Author(s):  
Hocine W. Mankouri ◽  
Hien-Ping Ngo ◽  
Ian D. Hickson

CSM2, PSY3, SHU1, and SHU2 (collectively referred to as the SHU genes) were identified in Saccharomyces cerevisiae as four genes in the same epistasis group that suppress various sgs1 and top3 mutant phenotypes when mutated. Although the SHU genes have been implicated in homologous recombination repair (HRR), their precise role(s) within this pathway remains poorly understood. Here, we have identified a specific role for the Shu proteins in a Rad51/Rad54-dependent HRR pathway(s) to repair MMS-induced lesions during S-phase. We show that, although mutation of RAD51 or RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising during replication in sgs1 cells, mutation of SHU genes attenuated the level of these structures. Similar findings were also observed in shu1 cells in which Rmi1 or Top3 function was impaired. We propose a model in which the Shu proteins act in HRR to promote the formation of HRR intermediates that are processed by the Sgs1-Rmi1-Top3 complex.


2014 ◽  
Vol 105 (7) ◽  
pp. 770-778 ◽  
Author(s):  
Xiaodong Jin ◽  
Yan Liu ◽  
Fei Ye ◽  
Xiongxiong Liu ◽  
Yoshiya Furusawa ◽  
...  

2012 ◽  
Vol 177 (5) ◽  
pp. 651-662 ◽  
Author(s):  
Lara Barazzuol ◽  
Raj Jena ◽  
Neil G. Burnet ◽  
Jonathan C. G. Jeynes ◽  
Michael J. Merchant ◽  
...  

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