scholarly journals N-(2'-deoxyguanosine-8-YL)-N-acetyl-2-aminofluorene induced translesion synthesis events in E.Coli: role of Y-family error-prone polymerases and the DNA sequence context

2004 ◽  
Author(s):  
M. Nokhbeh
Biochemistry ◽  
2003 ◽  
Vol 42 (8) ◽  
pp. 2456-2466 ◽  
Author(s):  
Xuanwei Huang ◽  
Alexander Kolbanovskiy ◽  
Xiaohua Wu ◽  
Yanbin Zhang ◽  
Zhigang Wang ◽  
...  

2008 ◽  
Vol 283 (51) ◽  
pp. 35569-35578 ◽  
Author(s):  
Yelena Margolin ◽  
Vladimir Shafirovich ◽  
Nicholas E. Geacintov ◽  
Michael S. DeMott ◽  
Peter C. Dedon

2018 ◽  
Vol 8 (2) ◽  
pp. 754-754
Author(s):  
Likui Zhang ◽  
Yanchao Huang ◽  
Xinyuan Zhu ◽  
Yuxiao Wang ◽  
Haoqiang Shi ◽  
...  

1988 ◽  
Vol 16 (17) ◽  
pp. 8351-8360 ◽  
Author(s):  
Beatrice Neuer-Nitsche ◽  
Xiang Lu ◽  
Dieter Werner

2018 ◽  
Vol 131 (12) ◽  
pp. jcs212183 ◽  
Author(s):  
Kiminori Kurashima ◽  
Takayuki Sekimoto ◽  
Tsukasa Oda ◽  
Tsuyoshi Kawabata ◽  
Fumio Hanaoka ◽  
...  

DNA Repair ◽  
2016 ◽  
Vol 46 ◽  
pp. 55-60 ◽  
Author(s):  
Keiji Hashimoto ◽  
Radha Bonala ◽  
Francis Johnson ◽  
Arthur P. Grollman ◽  
Masaaki Moriya

2009 ◽  
Vol 30 (3) ◽  
pp. 684-693 ◽  
Author(s):  
András Blastyák ◽  
Ildikó Hajdú ◽  
Ildikó Unk ◽  
Lajos Haracska

ABSTRACT Unrepaired DNA lesions can block the progression of the replication fork, leading to genomic instability and cancer in higher-order eukaryotes. In Saccharomyces cerevisiae, replication through DNA lesions can be mediated by translesion synthesis DNA polymerases, leading to error-free or error-prone damage bypass, or by Rad5-mediated template switching to the sister chromatid that is inherently error free. While translesion synthesis pathways are highly conserved from yeast to humans, very little is known of a Rad5-like pathway in human cells. Here we show that a human homologue of Rad5, HLTF, can facilitate fork regression and has a role in replication of damaged DNA. We found that HLTF is able to reverse model replication forks, a process which depends on its double-stranded DNA translocase activity. Furthermore, from analysis of isolated dually labeled chromosomal fibers, we demonstrate that in vivo, HLTF promotes the restart of replication forks blocked at DNA lesions. These findings suggest that HLTF can promote error-free replication of damaged DNA and support a role for HLTF in preventing mutagenesis and carcinogenesis, providing thereby for its potential tumor suppressor role.


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