Abstract
FoxO transcription factors are crucial modulators of various cellular processes, controlling the expression of target genes such as those coding for manganese superoxide dismutase (MnSOD) and selenoprotein P (SeP), thereby supporting defense against oxidative stress. Environmental stimuli such as heavy metal ions and polycyclic aromatic hydrocarbons (PAH) modulate signaling pathways both by interaction with proteins or by inducing the generation of reactive oxygen species (ROS). Exposure of hepatoma cells to nickel ions at subcytotoxic doses did not translate into modulation of FoxO activity despite an activation of the Ser/Thr-kinase Akt. The cellular response to nickel ions under these conditions is most likely independent of the formation of ROS, since there were no increased levels of glutathione disulfide detectable. FoxO activity was then found to be modulated in response to exposure of cells to PAH or the tryptophan photoproduct FICZ. Both PAH and FICZ caused an increased activity of a FoxO-responsive promoter construct as well as of glucose 6-phosphatase promoter activity. In contrast, the activities of promoters of genes coding for MnSOD or SeP were decreased in response to exposure to the PAH 3-methylcholanthrene (3-MC). In line with the promoter effects, 3-MC also decreased steady-state levels of SeP mRNA. The response
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Citation Formats
Eckers, Anna.
Regulation of FoxO transcription factors by environmental NO(x). Influence of metal ions and polycyclic aromatic hydrocarbons; Regulation von FoxO-Transkriptionsfaktoren durch Umweltnoxen. Einfluss von Metallionen und polyzyklischen aromatischen Kohlenwasserstoffen.
Germany: N. p.,
2009.
Web.
Eckers, Anna.
Regulation of FoxO transcription factors by environmental NO(x). Influence of metal ions and polycyclic aromatic hydrocarbons; Regulation von FoxO-Transkriptionsfaktoren durch Umweltnoxen. Einfluss von Metallionen und polyzyklischen aromatischen Kohlenwasserstoffen.
Germany.
Eckers, Anna.
2009.
"Regulation of FoxO transcription factors by environmental NO(x). Influence of metal ions and polycyclic aromatic hydrocarbons; Regulation von FoxO-Transkriptionsfaktoren durch Umweltnoxen. Einfluss von Metallionen und polyzyklischen aromatischen Kohlenwasserstoffen."
Germany.
@misc{etde_21422792,
title = {Regulation of FoxO transcription factors by environmental NO(x). Influence of metal ions and polycyclic aromatic hydrocarbons; Regulation von FoxO-Transkriptionsfaktoren durch Umweltnoxen. Einfluss von Metallionen und polyzyklischen aromatischen Kohlenwasserstoffen}
author = {Eckers, Anna}
abstractNote = {FoxO transcription factors are crucial modulators of various cellular processes, controlling the expression of target genes such as those coding for manganese superoxide dismutase (MnSOD) and selenoprotein P (SeP), thereby supporting defense against oxidative stress. Environmental stimuli such as heavy metal ions and polycyclic aromatic hydrocarbons (PAH) modulate signaling pathways both by interaction with proteins or by inducing the generation of reactive oxygen species (ROS). Exposure of hepatoma cells to nickel ions at subcytotoxic doses did not translate into modulation of FoxO activity despite an activation of the Ser/Thr-kinase Akt. The cellular response to nickel ions under these conditions is most likely independent of the formation of ROS, since there were no increased levels of glutathione disulfide detectable. FoxO activity was then found to be modulated in response to exposure of cells to PAH or the tryptophan photoproduct FICZ. Both PAH and FICZ caused an increased activity of a FoxO-responsive promoter construct as well as of glucose 6-phosphatase promoter activity. In contrast, the activities of promoters of genes coding for MnSOD or SeP were decreased in response to exposure to the PAH 3-methylcholanthrene (3-MC). In line with the promoter effects, 3-MC also decreased steady-state levels of SeP mRNA. The response of the SeP promoter to 3-MC was abrogated by point mutations introduced at the two identified FoxO binding elements of the SeP promoter, implying that interaction of FoxO proteins with these sites is essential for the downregulation of promoter activity. In addition to FoxO activity being modulated by xenobiotics, it was then demonstrated that FoxO expression was also modulated by exposure of cells to PAH or FICZ. FoxO4 mRNA levels were downregulated in hepatoma cells exposed to 3-MC or FICZ. Similarly, insulin treatment caused a downregulation of mRNA levels of FoxO 1a, 3a and 4 in hepatoma cells. (orig.)}
place = {Germany}
year = {2009}
month = {Dec}
}
title = {Regulation of FoxO transcription factors by environmental NO(x). Influence of metal ions and polycyclic aromatic hydrocarbons; Regulation von FoxO-Transkriptionsfaktoren durch Umweltnoxen. Einfluss von Metallionen und polyzyklischen aromatischen Kohlenwasserstoffen}
author = {Eckers, Anna}
abstractNote = {FoxO transcription factors are crucial modulators of various cellular processes, controlling the expression of target genes such as those coding for manganese superoxide dismutase (MnSOD) and selenoprotein P (SeP), thereby supporting defense against oxidative stress. Environmental stimuli such as heavy metal ions and polycyclic aromatic hydrocarbons (PAH) modulate signaling pathways both by interaction with proteins or by inducing the generation of reactive oxygen species (ROS). Exposure of hepatoma cells to nickel ions at subcytotoxic doses did not translate into modulation of FoxO activity despite an activation of the Ser/Thr-kinase Akt. The cellular response to nickel ions under these conditions is most likely independent of the formation of ROS, since there were no increased levels of glutathione disulfide detectable. FoxO activity was then found to be modulated in response to exposure of cells to PAH or the tryptophan photoproduct FICZ. Both PAH and FICZ caused an increased activity of a FoxO-responsive promoter construct as well as of glucose 6-phosphatase promoter activity. In contrast, the activities of promoters of genes coding for MnSOD or SeP were decreased in response to exposure to the PAH 3-methylcholanthrene (3-MC). In line with the promoter effects, 3-MC also decreased steady-state levels of SeP mRNA. The response of the SeP promoter to 3-MC was abrogated by point mutations introduced at the two identified FoxO binding elements of the SeP promoter, implying that interaction of FoxO proteins with these sites is essential for the downregulation of promoter activity. In addition to FoxO activity being modulated by xenobiotics, it was then demonstrated that FoxO expression was also modulated by exposure of cells to PAH or FICZ. FoxO4 mRNA levels were downregulated in hepatoma cells exposed to 3-MC or FICZ. Similarly, insulin treatment caused a downregulation of mRNA levels of FoxO 1a, 3a and 4 in hepatoma cells. (orig.)}
place = {Germany}
year = {2009}
month = {Dec}
}