Research Topics
| Travis J O'BrienSummaryAffiliation: The George Washington University Country: USA Publications
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Detail Information
Publications
DNA polymerase zeta is essential for hexavalent chromium-induced mutagenesisTravis J O'Brien
Department of Pharmacology and Physiology, The George Washington University, Washington, DC 20037, USA
Mutat Res 663:77-83. 2009..This work provides novel information regarding the molecular mechanisms of Cr(VI)-induced mutagenesis and is the first report demonstrating a role for TLS in the fixation of mutations induced by a carcinogenic metal...
Development of an undergraduate pharmacogenomics curriculumTravis J O'Brien
The George Washington University Medical Center, Ross Hall Room 660A, 2300 Eye Street, NW, Washington, DC 20037, USA
Pharmacogenomics 10:1979-86. 2009..This course offers the advantage of exposing students to the concepts of pharmacogenomics prior to their enrollment in PhD, PharmD or MD/DO graduate programs...
Nucleotide excision repair functions in the removal of chromium-induced DNA damage in mammalian cellsTravis J O'Brien
Department of Pharmacology and Physiology, The George Washington University Medical Center, Washington, DC 20037, USA
Mol Cell Biochem 279:85-95. 2005..Consequently, NER may represent an important mechanism for preventing Cr(VI)-induced mutagenesis and neoplastic transformation...
Incision of trivalent chromium [Cr(III)]-induced DNA damage by Bacillus caldotenax UvrABC endonucleaseTravis J O'Brien
Department of Pharmacology and Physiology, The George Washington University, Washington, DC 20037, United States
Mutat Res 610:85-92. 2006..Taken together, our data suggest that a sub-fraction of Cr(III)-DNA adducts is recognized and processed by the prokaryotic NER machinery and that ICLs are not necessarily the sole lesions generated by Cr(III) that are substrates for NER...
Excision repair is required for genotoxin-induced mutagenesis in mammalian cellsBradford Brooks
Department of Pharmacology and Physiology, The George Washington University Medical Center, 2300 Eye Street Northwest, Washington, DC 20037, USA
Carcinogenesis 29:1064-9. 2008..We postulate that, in the absence of ER, DNA damage is channeled into an error-free system of DNA repair or damage tolerance...
Polo-like kinase 1 enhances survival and mutagenesis after genotoxic stress in normal cells through cell cycle checkpoint bypassGina Chun
Department of Pharmacology and Physiology, The George Washington University Medical Center, Washington, DC 20037, USA
Carcinogenesis 31:785-93. 2010..Our studies highlight a role for Plk1 in the loss of checkpoint control, increased survival and mutagenesis after genotoxic exposure in normal cells, which in turn may lead to genomic instability and carcinogenesis...
Effects of hexavalent chromium on the survival and cell cycle distribution of DNA repair-deficient S. cerevisiaeTravis J O'Brien
Molecular and Cellular Oncology Program, Department of Pharmacology, The George Washington University Medical Center, Washington, DC 20037, USA
DNA Repair (Amst) 1:617-27. 2002..Furthermore, only the combined inactivation of multiple excision repair genes affects cell growth after Cr(VI) treatment...
Bypass of hexavalent chromium-induced growth arrest by a protein tyrosine phosphatase inhibitor: enhanced survival and mutagenesisDongsoon Bae
Department of Pharmacology and Physiology, The George Washington University Medical Center, Washington, DC, USA
Mutat Res 660:40-6. 2009....
