Louise M Winn

Summary

Affiliation: Queen's University
Country: Canada

Publications

  1. ncbi Pim-1 phosphorylates the DNA binding domain of c-Myb
    Louise M Winn
    Department of Pharmacology and Toxicology, Botterell Hall, Queen s University, Kingston, Ontario K7L 3N6, Canada
    Cell Cycle 2:258-62. 2003
  2. ncbi Valproic acid increases conservative homologous recombination frequency and reactive oxygen species formation: a potential mechanism for valproic acid-induced neural tube defects
    Ericka N Defoort
    Department of Pharmacology and Toxicology and School of Environmental Studies, Queen s University, Kingston, Ontario, Canada
    Mol Pharmacol 69:1304-10. 2006
  3. ncbi Homologous recombination initiated by benzene metabolites: a potential role of oxidative stress
    Louise M Winn
    Department of Pharmacology and Toxicology, Queen s University, Kingston K7L 3N6, Ontario, Canada
    Toxicol Sci 72:143-9. 2003
  4. ncbi Oxidative stress-induced homologous recombination as a novel mechanism for phenytoin-initiated toxicity
    Louise M Winn
    Department of Pharmacology and Toxicology and School of Environmental Studies, Queen s University, Kingston, ON, Canada
    J Pharmacol Exp Ther 306:523-7. 2003
  5. ncbi Benzene's metabolites alter c-MYB activity via reactive oxygen species in HD3 cells
    Joanne Wan
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Toxicol Appl Pharmacol 222:180-9. 2007
  6. doi Characterization of valproic acid-initiated homologous recombination
    Kevin Sha
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Birth Defects Res B Dev Reprod Toxicol 89:124-32. 2010
  7. ncbi TCDD-induced homologous recombination: the role of the Ah receptor versus oxidative DNA damage
    Clara Y Y Chan
    Department of Pharmacology and Toxicology, Botterell Hall Room 557, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Mutat Res 563:71-9. 2004
  8. doi In utero exposure to benzene disrupts fetal hematopoietic progenitor cell growth via reactive oxygen species
    Helen J Badham
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Toxicol Sci 113:207-15. 2010
  9. doi The effects of 1,4-benzoquinone on c-Myb and topoisomerase II in K-562 cells
    Roopam Singh
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Mutat Res 645:33-8. 2008
  10. doi In utero and in vitro effects of benzene and its metabolites on erythroid differentiation and the role of reactive oxygen species
    Helen J Badham
    Department of Pharmacology and Toxicology Queen s University, Kingston, Ontario, Canada K7L 3N6
    Toxicol Appl Pharmacol 244:273-9. 2010

Collaborators

Detail Information

Publications31

  1. ncbi Pim-1 phosphorylates the DNA binding domain of c-Myb
    Louise M Winn
    Department of Pharmacology and Toxicology, Botterell Hall, Queen s University, Kingston, Ontario K7L 3N6, Canada
    Cell Cycle 2:258-62. 2003
    ..Pim-1 associated with Myb both in cells and in vitro, and phosphorylated the Myb DNA binding domain, suggesting that it regulates Myb protein activity by direct phosphorylation...
  2. ncbi Valproic acid increases conservative homologous recombination frequency and reactive oxygen species formation: a potential mechanism for valproic acid-induced neural tube defects
    Ericka N Defoort
    Department of Pharmacology and Toxicology and School of Environmental Studies, Queen s University, Kingston, Ontario, Canada
    Mol Pharmacol 69:1304-10. 2006
    ..These data demonstrate that valproic acid increases HR frequency and provides a possible mechanism for valproic acid-induced neural tube defects...
  3. ncbi Homologous recombination initiated by benzene metabolites: a potential role of oxidative stress
    Louise M Winn
    Department of Pharmacology and Toxicology, Queen s University, Kingston K7L 3N6, Ontario, Canada
    Toxicol Sci 72:143-9. 2003
    ..These data support the hypothesis that increased homologous recombination mediates benzene-initiated toxicity and supports a role for oxidative stress in this mechanism...
  4. ncbi Oxidative stress-induced homologous recombination as a novel mechanism for phenytoin-initiated toxicity
    Louise M Winn
    Department of Pharmacology and Toxicology and School of Environmental Studies, Queen s University, Kingston, ON, Canada
    J Pharmacol Exp Ther 306:523-7. 2003
    ..Our data demonstrate that phenytoin-initiated DNA damage can induce homologous recombination, which may be a novel mechanism mediating phenytoin-initiated toxicity...
  5. ncbi Benzene's metabolites alter c-MYB activity via reactive oxygen species in HD3 cells
    Joanne Wan
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Toxicol Appl Pharmacol 222:180-9. 2007
    ..More importantly, this study supports the hypothesis that benzene may mediate its toxicity through ROS-mediated alterations in the c-Myb signaling pathway...
  6. doi Characterization of valproic acid-initiated homologous recombination
    Kevin Sha
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Birth Defects Res B Dev Reprod Toxicol 89:124-32. 2010
    ..We have also shown that VPA exposure leads to both an increase in reactive oxygen species (ROS) production and increased frequency of homologous recombination (HR)...
  7. ncbi TCDD-induced homologous recombination: the role of the Ah receptor versus oxidative DNA damage
    Clara Y Y Chan
    Department of Pharmacology and Toxicology, Botterell Hall Room 557, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Mutat Res 563:71-9. 2004
    ..These results suggest that TCDD-initiated homologous recombination in CHO 3-6 cells is mediated by the AhR and not via increased oxidative stress...
  8. doi In utero exposure to benzene disrupts fetal hematopoietic progenitor cell growth via reactive oxygen species
    Helen J Badham
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Toxicol Sci 113:207-15. 2010
    ..These results suggest that ROS play a key role in the development of in utero-initiated benzene toxicity potentially through disruption of hematopoietic cell signaling pathways...
  9. doi The effects of 1,4-benzoquinone on c-Myb and topoisomerase II in K-562 cells
    Roopam Singh
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Mutat Res 645:33-8. 2008
    ....
  10. doi In utero and in vitro effects of benzene and its metabolites on erythroid differentiation and the role of reactive oxygen species
    Helen J Badham
    Department of Pharmacology and Toxicology Queen s University, Kingston, Ontario, Canada K7L 3N6
    Toxicol Appl Pharmacol 244:273-9. 2010
    ..In conclusion, this study provided evidence that ROS generated as a result of benzene metabolism may significantly alter erythroid differentiation, potentially leading to the development of Blood Disorders...
  11. doi Benzene-initiated oxidative stress: Effects on embryonic signaling pathways
    Helen J Badham
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Chem Biol Interact 184:218-21. 2010
    ..Further studies evaluating the reason for this gender difference are ongoing...
  12. doi In utero exposure to benzene increases embryonic c-Myb and Pim-1 protein levels in CD-1 mice
    Joanne Wan
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Toxicol Appl Pharmacol 228:326-33. 2008
    ..These results support a role for ROS in c-Myb and Pim-1 alterations after in utero benzene exposure...
  13. ncbi Benzo[a]pyrene increases DNA double strand break repair in vitro and in vivo: a possible mechanism for benzo[a]pyrene-induced toxicity
    Emily W Y Tung
    Department of Biomedical and Molecular Sciences, Graduate Program in Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Mutat Res Genet Toxicol Environ Mutagen 760:64-9. 2014
    ..As repair of DNA DSBs is not error-free, aberrant DNA repair may be contributing to the mechanism of BaP-induced toxicity. ..
  14. doi DNA double-strand breaks and DNA recombination in benzene metabolite-induced genotoxicity
    Emily W Y Tung
    Department of Biomedical and Molecular Sciences, Queen s University, Room 557, Botterell Hall, Kingston, Ontario K7L 3N6, Canada
    Toxicol Sci 126:569-77. 2012
    ..These studies indicate that BQ is able to induce DNA damage and recombination in fetal liver cells and that ROS may be important in the mechanism of toxicity...
  15. doi Valproic acid-induced DNA damage increases embryonic p27(KIP1) and caspase-3 expression: a mechanism for valproic-acid induced neural tube defects
    Emily W Y Tung
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Reprod Toxicol 32:255-60. 2011
    ..Immunohistochemistry revealed increased staining for γH2A.X, p27(KIP1), and cleaved caspase 3 in the head, confirming our hypothesis that DNA damage, cell cycle inhibition, and apoptosis are induced by VPA...
  16. doi The effect of TiO(2) and Ag nanoparticles on reproduction and development of Drosophila melanogaster and CD-1 mice
    Nicola A Philbrook
    School of Environmental Studies, Biosciences Complex, Queen s University, 116 Barrie Street, Kingston, Ontario, Canada K7L 3N6
    Toxicol Appl Pharmacol 257:429-36. 2011
    ..Taken together, however, this study warns that these common NPs could be detrimental to the reproductive and developmental health of both invertebrates and vertebrates...
  17. ncbi The effects of benzene and the metabolites phenol and catechol on c-Myb and Pim-1 signaling in HD3 cells
    Joanne Wan
    Department of Pharmacology and Toxicology, Queen s University, Kingston, ON, Canada K7L 3N6
    Toxicol Appl Pharmacol 201:194-201. 2004
    ..More importantly, this study supports the hypothesis that benzene may mediate its toxicity through metabolite-mediated alterations in the c-Myb signaling pathway...
  18. doi Valproic acid increases formation of reactive oxygen species and induces apoptosis in postimplantation embryos: a role for oxidative stress in valproic acid-induced neural tube defects
    Emily W Y Tung
    Department of Biomedical and Molecular Sciences, Graduate Program in Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada
    Mol Pharmacol 80:979-87. 2011
    ..These studies identify regions of the embryo susceptible to ROS and apoptosis induced by VPA, thus establishing a possible molecular pathway by which VPA exerts teratogenicity...
  19. doi Assessment of xenobiotic biotransformation including reactive oxygen species generation in the embryo using benzene as an example
    Helen J Renaud
    Department of Pharmacology and Toxicology, Queen s University, Kingston, ON, Canada
    Methods Mol Biol 889:253-63. 2012
    ....
  20. doi Epigenetic modifications in valproic acid-induced teratogenesis
    Emily W Y Tung
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario K7L3N6, Canada
    Toxicol Appl Pharmacol 248:201-9. 2010
    ..These results support the possibility that epigenetic modifications caused by VPA during early mouse organogenesis results in congenital malformations...
  21. ncbi Investigating the role of the aryl hydrocarbon receptor in benzene-initiated toxicity in vitro
    Helen J Badham
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario K7L 3N6, Canada
    Toxicology 229:177-85. 2007
    ..These results indicate that the involvement of the AhR in benzene toxicity does not seem to be through classical activation of this receptor or through interference of oxidative stress pathways...
  22. ncbi Thalidomide alters c-MYB and PIM-1 signaling in K-562 cells
    Natasha A Thadani
    Department of Pharmacology, School of Environmental Studies, Queen s University, Botterell Hall Room 557, Kingston, Ont, Canada K7L 3N6
    Pharmacol Res 54:91-6. 2006
    ..Together these results demonstrate that thalidomide affects c-Myb signaling, in part, through increased ROS production...
  23. ncbi Transplacental benzene exposure increases tumor incidence in mouse offspring: possible role of fetal benzene metabolism
    Helen J Badham
    Department of Pharmacology and Toxicology, Queen s Cancer Research Institute, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Carcinogenesis 31:1142-8. 2010
    ..This is the first demonstration that transplacental benzene exposure can induce hepatic and hematopoietic tumors in mice, which may be dependent on fetal benzene metabolism capability...
  24. ncbi TCDD affects DNA double strand-break repair
    Clara Y Y Chan
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada 27L3N6
    Toxicol Sci 81:133-8. 2004
    ..Exposure of cells to alpha-naphthoflavone resulted in a significant decrease in TCDD-induced HR frequency. These results demonstrate that TCDD, potentially acting via the AhR, can modulate HR repair of DNA DSBs in CHO 33 cells...
  25. ncbi In utero-initiated cancer: the role of reactive oxygen species
    Joanne Wan
    Department of Pharmacology and Toxicology, School of Environmental Studies, Queen s University, Kingston, Ontario, Canada
    Birth Defects Res C Embryo Today 78:326-32. 2006
    ..Using a number of examples, this review will focus on the role of reactive oxygen species (ROS) in the mechanisms pertaining to in utero initiated cancers...
  26. doi Assessment of embryotoxicity using mouse embryo culture
    Louise M Winn
    Department of Pharmacology and School of Environmental Studies, Queen s University, Kingston, Ontario, Canada
    Methods Mol Biol 550:241-9. 2009
    ..Additional biochemical analysis, including molecular approaches to assess embryonic signal transduction, as well as some limitations of the technique will also be discussed...
  27. doi In utero and acute exposure to benzene: investigation of DNA double-strand breaks and DNA recombination in mice
    Annette Lau
    Department of Pharmacology and Toxicology, Queen s University, Kingston, Ontario, Canada, K7L3N6
    Mutat Res 676:74-82. 2009
    ..Further investigations into different types of DNA damage and repair pathways are warranted to fully elucidate the role of genotoxic mechanisms in the etiology of benzene-induced childhood leukemias...
  28. ncbi Folic acid and pantothenic acid protection against valproic acid-induced neural tube defects in CD-1 mice
    Jennifer E Dawson
    Department of Pharmacology and Toxicology and School of Environmental Studies, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Toxicol Appl Pharmacol 211:124-32. 2006
    ....
  29. doi Investigating the effects of functionalized carbon nanotubes on reproduction and development in Drosophila melanogaster and CD-1 mice
    Nicola A Philbrook
    School of Environmental Studies, Biosciences Complex, Queen s University, 116 Barrie Street, Kingston, Ontario, Canada
    Reprod Toxicol 32:442-8. 2011
    ..This research underscores the need to examine the effects of fCNTs on reproductive health and development before the opportunities for maternal exposure by fCNTs increase further...
  30. doi Sub-chronic sulforaphane exposure in CD-1 pregnant mice enhances maternal NADPH quinone oxidoreductase 1 (NQO1) activity and mRNA expression of NQO1, glutathione S-transferase, and glutamate-cysteine ligase: potential implications for fetal protection aga
    Nicola A Philbrook
    Department of Biomedical and Molecular Sciences, Graduate Program in Pharmacology and Toxicology Graduate Program, Queen s University, Kingston, Ontario, Canada K7L 3N6
    Reprod Toxicol 43:30-7. 2014
    ..Demonstration that SFN induces maternal gene expression and activity supports further investigation of SFN as a preventative agent against transplacental toxicity...
  31. ncbi Evidence for Ras-dependent signal transduction in phenytoin teratogenicity
    Louise M Winn
    Faculty of Pharmacy, University of Toronto, Toronto, Ontario, M5S 2S2, Canada
    Toxicol Appl Pharmacol 184:144-52. 2002
    ..These results provide the first direct evidence that Ras proteins may be involved in the teratogenicity of phenytoin, likely via a mechanism other than mutational activation...