Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA060836-04
Application #
2101607
Study Section
Experimental Therapeutics Subcommittee 1 (ET)
Project Start
1993-07-06
Project End
1998-04-30
Budget Start
1996-05-01
Budget End
1997-04-30
Support Year
4
Fiscal Year
1996
Total Cost
Indirect Cost
Name
Duke University
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
071723621
City
Durham
State
NC
Country
United States
Zip Code
27705
Newmark, Kathryn G; O'Reilly, Erin K; Pohlhaus, Jennifer Reineke et al. (2005) Genetic analysis of the requirements for SOS induction by nalidixic acid in Escherichia coli. Gene 356:69-76
O'Reilly, Erin K; Kreuzer, Kenneth N (2004) Isolation of SOS constitutive mutants of Escherichia coli. J Bacteriol 186:7149-60
Hong, George; Kreuzer, Kenneth N (2003) Endonuclease cleavage of blocked replication forks: An indirect pathway of DNA damage from antitumor drug-topoisomerase complexes. Proc Natl Acad Sci U S A 100:5046-51
O'Reilly, Erin K; Kreuzer, Kenneth N (2002) A unique type II topoisomerase mutant that is hypersensitive to a broad range of cleavage-inducing antitumor agents. Biochemistry 41:7989-97
Kreuzer, K N; Freudenreich, C H; Pommier, Y (2001) Analysis of cleavage complexes using reactive inhibitor derivatives. Methods Mol Biol 95:89-99
Stohr, B A; Kreuzer, K N (2001) Repair of topoisomerase-mediated DNA damage in bacteriophage T4. Genetics 158:19-28
Hong, G; Kreuzer, K N (2000) An antitumor drug-induced topoisomerase cleavage complex blocks a bacteriophage T4 replication fork in vivo. Mol Cell Biol 20:594-603
Kreuzer, K N (2000) Recombination-dependent DNA replication in phage T4. Trends Biochem Sci 25:165-73
Kreuzer, K N (1998) Bacteriophage T4, a model system for understanding the mechanism of type II topoisomerase inhibitors. Biochim Biophys Acta 1400:339-47
Freudenreich, C H; Chang, C; Kreuzer, K N (1998) Mutations of the bacteriophage T4 type II DNA topoisomerase that alter sensitivity to antitumor agent 4'-(9-acridinylamino)methanesulfon-m-anisidide and an antibacterial quinolone. Cancer Res 58:1260-7

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