Corrigendum to “Non-specific DNA binding interferes with the efficient excision of oxidative lesions from chromatin by the human DNA glycosylase, NEIL1” [DNA Repair 9 (2010) 134–143]

DNA Repair ◽  
2010 ◽  
Vol 9 (8) ◽  
pp. 938 ◽  
Author(s):  
Ian D. Odell ◽  
Kheng Newick ◽  
Nicholas H. Heintz ◽  
Susan S. Wallace ◽  
David S. Pederson
Biochemistry ◽  
1999 ◽  
Vol 38 (29) ◽  
pp. 9417-9425 ◽  
Author(s):  
Sandra L. McCutchen-Maloney ◽  
Cindi A. Giannecchini ◽  
Mona H. Hwang ◽  
Michael P. Thelen

DNA Repair ◽  
2010 ◽  
Vol 9 (2) ◽  
pp. 134-143 ◽  
Author(s):  
Ian D. Odell ◽  
Kheng Newick ◽  
Nicholas H. Heintz ◽  
Susan S. Wallace ◽  
David S. Pederson

2004 ◽  
Vol 11 (8) ◽  
pp. 714-720 ◽  
Author(s):  
Douglas S Daniels ◽  
Tammy T Woo ◽  
Kieu X Luu ◽  
David M Noll ◽  
Neil D Clarke ◽  
...  

Genetics ◽  
1998 ◽  
Vol 148 (4) ◽  
pp. 1441-1451
Author(s):  
Johan G de Boer ◽  
Barry W Glickman

Abstract The lacI gene has been used extensively for the recovery and analysis of mutations in bacteria with various DNA repair backgrounds and after exposure to a wide variety of mutagens. This has resulted in a large database of information on mutational mechanisms and specificity of many mutagens, as well as the effect of DNA repair background on mutagenicity. Most importantly, knowledge about the mutational sensitivity of the lacI gene is now available, yielding information about mutable nucleotides. This popularity and available knowledge resulted in the use of the lacI gene in transgenic rodents for the study of mutagenesis in mammals, where it resides in ~40 repeated copies. As the number of sequenced mutations recovered from these animals increases, we are able to analyze the sites at which mutations have been recovered in great detail and to compare the recovered sites between bacteria and transgenic animals. The nucleotides that code for the DNA-binding domain are nearly saturated with base substitutions. Even after determining the sequences of ~10,000 mutations recovered from the animals, however, new sites and new changes are still being recovered. In addition, we compare the nature of deletion mutations between bacteria and animals. Based on the nature of deletions in the animals, we conclude that each deletion occurs in a single copy of the gene.


1985 ◽  
Vol 5 (2) ◽  
pp. 398-405 ◽  
Author(s):  
J S Rubin ◽  
V R Prideaux ◽  
H F Willard ◽  
A M Dulhanty ◽  
G F Whitmore ◽  
...  

The genes and gene products involved in the mammalian DNA repair processes have yet to be identified. Toward this end we made use of a number of DNA repair-proficient transformants that were generated after transfection of DNA from repair-proficient human cells into a mutant hamster line that is defective in the initial incision step of the excision repair process. In this report, biochemical evidence is presented that demonstrates that these transformants are repair proficient. In addition, we describe the molecular identification and cloning of unique DNA sequences closely associated with the transfected human DNA repair gene and demonstrate the presence of homologous DNA sequences in human cells and in the repair-proficient DNA transformants. The chromosomal location of these sequences was determined by using a panel of rodent-human somatic cell hybrids. Both unique DNA sequences were found to be on human chromosome 19.


2011 ◽  
Vol 12 (1) ◽  
pp. 4 ◽  
Author(s):  
Caroline Smet-Nocca ◽  
Jean-Michel Wieruszeski ◽  
Hélène Léger ◽  
Sebastian Eilebrecht ◽  
Arndt Benecke

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