Travis J O'Brien

Summary

Affiliation: The George Washington University
Country: USA

Publications

  1. pmc DNA polymerase zeta is essential for hexavalent chromium-induced mutagenesis
    Travis J O'Brien
    Department of Pharmacology and Physiology, The George Washington University, Washington, DC 20037, USA
    Mutat Res 663:77-83. 2009
  2. doi request reprint Development of an undergraduate pharmacogenomics curriculum
    Travis 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
  3. ncbi request reprint Effects of hexavalent chromium on the survival and cell cycle distribution of DNA repair-deficient S. cerevisiae
    Travis 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
  4. ncbi request reprint Nucleotide excision repair functions in the removal of chromium-induced DNA damage in mammalian cells
    Travis 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
  5. ncbi request reprint Incision of trivalent chromium [Cr(III)]-induced DNA damage by Bacillus caldotenax UvrABC endonuclease
    Travis J O'Brien
    Department of Pharmacology and Physiology, The George Washington University, Washington, DC 20037, United States
    Mutat Res 610:85-92. 2006
  6. pmc Resistance to apoptosis, increased growth potential, and altered gene expression in cells that survived genotoxic hexavalent chromium [Cr(VI)] exposure
    Daryl E Pritchard
    The George Washington University Medical Center, Washington, DC 20037, USA
    Mol Cell Biochem 279:169-81. 2005
  7. ncbi request reprint Differential impact of ionic and coordinate covalent chromium (Cr)-DNA binding on DNA replication
    Jamie L Fornsaglio
    Department of Pharmacology and Physiology, The George Washington University Medical Center, Washington, DC 20037, USA
    Mol Cell Biochem 279:149-55. 2005
  8. pmc Excision repair is required for genotoxin-induced mutagenesis in mammalian cells
    Bradford 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
  9. pmc Polo-like kinase 1 enhances survival and mutagenesis after genotoxic stress in normal cells through cell cycle checkpoint bypass
    Gina Chun
    Department of Pharmacology and Physiology, The George Washington University Medical Center, Washington, DC 20037, USA
    Carcinogenesis 31:785-93. 2010
  10. ncbi request reprint Complexities of chromium carcinogenesis: role of cellular response, repair and recovery mechanisms
    Travis J O'Brien
    Department of Pharmacology and Molecular and Cellular Oncology Program, The George Washington University Medical Center, 2300 I Street NW, Washington, DC 20037, USA
    Mutat Res 533:3-36. 2003

Collaborators

Detail Information

Publications19

  1. pmc DNA polymerase zeta is essential for hexavalent chromium-induced mutagenesis
    Travis 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...
  2. doi request reprint Development of an undergraduate pharmacogenomics curriculum
    Travis 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...
  3. ncbi request reprint Effects of hexavalent chromium on the survival and cell cycle distribution of DNA repair-deficient S. cerevisiae
    Travis 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...
  4. ncbi request reprint Nucleotide excision repair functions in the removal of chromium-induced DNA damage in mammalian cells
    Travis 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...
  5. ncbi request reprint Incision of trivalent chromium [Cr(III)]-induced DNA damage by Bacillus caldotenax UvrABC endonuclease
    Travis 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...
  6. pmc Resistance to apoptosis, increased growth potential, and altered gene expression in cells that survived genotoxic hexavalent chromium [Cr(VI)] exposure
    Daryl E Pritchard
    The George Washington University Medical Center, Washington, DC 20037, USA
    Mol Cell Biochem 279:169-81. 2005
    ..Selection of cells with altered expression of these genes may constitute the early stages of tumour progression...
  7. ncbi request reprint Differential impact of ionic and coordinate covalent chromium (Cr)-DNA binding on DNA replication
    Jamie L Fornsaglio
    Department of Pharmacology and Physiology, The George Washington University Medical Center, Washington, DC 20037, USA
    Mol Cell Biochem 279:149-55. 2005
    ..Thus, these results suggest that treatment of living cells with Cr(VI) leads to two modes of Cr-binding, which may have conflicting effects on DNA replication...
  8. pmc Excision repair is required for genotoxin-induced mutagenesis in mammalian cells
    Bradford 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...
  9. pmc Polo-like kinase 1 enhances survival and mutagenesis after genotoxic stress in normal cells through cell cycle checkpoint bypass
    Gina 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...
  10. ncbi request reprint Complexities of chromium carcinogenesis: role of cellular response, repair and recovery mechanisms
    Travis J O'Brien
    Department of Pharmacology and Molecular and Cellular Oncology Program, The George Washington University Medical Center, 2300 I Street NW, Washington, DC 20037, USA
    Mutat Res 533:3-36. 2003
    ..These pertinent issues must be considered in relation to the potential role that each plays in the induction of human respiratory tract cancer by particulate Cr(VI) compounds...
  11. pmc Fanconi anemia complementation group A cells are hypersensitive to chromium(VI)-induced toxicity
    Susan K Vilcheck
    Department of Pharmacology, Program in Molecular and Cellular Oncology, The George Washington University Medical Center, 2300 Eye Street NW, Washington, DC 20037, USA
    Environ Health Perspect 110:773-7. 2002
    ..The results also suggest that Cr-DDC may be proapoptotic lesions. These results are the first to show that FA cells are hypersensitive to an environmentally relevant DNA cross-linking agent...
  12. pmc FANCD2 monoubiquitination and activation by hexavalent chromium [Cr(VI)] exposure: activation is not required for repair of Cr(VI)-induced DSBs
    Susan K Vilcheck
    Department of Pharmacology and Physiology, The George Washington University Medical Center, 2300 Eye Street, NW, Washington, DC 20037, United States
    Mutat Res 610:21-30. 2006
    ..While previous research on FA has defined the genetic causes of this disease, it is critical in terms of individual risk assessment to address how cells from FA patients respond to genotoxic insult...
  13. ncbi request reprint Hypoxia impedes the formation of chromium DNA-adducts in a cell-free system
    Travis J O'Brien
    Department of Pharmacology and Physiology, The George Washington University Medical Center, 2300 Eye Street NW, Washington, DC 20037, USA
    Biochem Pharmacol 70:1814-22. 2005
    ..Taken together, these results support a role for dioxygen in facilitating the formation of Cr-DNA coordination complexes...
  14. pmc Bypass of hexavalent chromium-induced growth arrest by a protein tyrosine phosphatase inhibitor: enhanced survival and mutagenesis
    Dongsoon Bae
    Department of Pharmacology and Physiology, The George Washington University Medical Center, Washington, DC, USA
    Mutat Res 660:40-6. 2009
    ....
  15. ncbi request reprint Mechanisms of chromium-induced suppression of RNA synthesis in cellular and cell-free systems: relationship to RNA polymerase arrest
    Jian Xu
    Department of Pharmacology, The George Washington University Medical Center, Washington, DC 20037, USA
    Mol Cell Biochem 255:151-60. 2004
    ..Taken together, these results suggest that the suppression of RNA synthesis by Cr is related to chromium-induced template DNA damage which prevents elongation leading to premature RNA polymerase arrest...
  16. pmc Kinase insert domain receptor/vascular endothelial growth factor receptor 2 (KDR) genetic variation is associated with ovarian hyperstimulation syndrome
    Travis J O'Brien
    Department of Pharmacology and Physiology, The George Washington University, Washington, DC, USA
    Reprod Biol Endocrinol 12:36. 2014
    ....
  17. ncbi request reprint First report of warfarin dose requirements in patients possessing the CYP2C9*12 allele
    Travis J O'Brien
    The George Washington University, Department of Pharmacology and Physiology, Washington, DC, United States
    Clin Chim Acta 424:73-5. 2013
    ..Numerous variant alleles of CYP2C9 have been identified. The CYP2C9*12 (rs9332239) allele harbors a P489S substitution in CYP2C9 which has been shown to result in a 40% decline in catalytic activity in vitro...
  18. doi request reprint Assessment of K-Ras mutant frequency and micronucleus incidence in the mouse duodenum following 90-days of exposure to Cr(VI) in drinking water
    Travis J O'Brien
    George Washington University, Department of Pharmacology and Physiology, Washington, DC 20037, United States
    Mutat Res 754:15-21. 2013
    ....
  19. doi request reprint The current and future state of pharmacogenomics medical education in the USA
    Tracey J Nickola
    Department of Pharmacology and Physiology, Pharmacogenomics Program, The George Washington University, Ross Hall Room 660A, 2300 Eye Street, NW Washington, DC 20037, USA
    Pharmacogenomics 13:1419-25. 2012
    ..Based on our experience as undergraduate and pharmacy PGx educators, we further reflect on our experience educating future healthcare professionals on PGx...