Christoph Franz Adam Vogel

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Combustion-derived flame generated ultrafine soot generates reactive oxygen species and activates Nrf2 antioxidants differently in neonatal and adult rat lungs
    Jackie K W Chan
    Center for Health and the Environment, University of California, One Shields Ave, Davis, CA 95616, USA
    Part Fibre Toxicol 10:34. 2013
  2. pmc Activation of inflammatory responses in human U937 macrophages by particulate matter collected from dairy farms: an in vitro expression analysis of pro-inflammatory markers
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
    Environ Health 11:17. 2012
  3. pmc Characterization of MCF mammary epithelial cells overexpressing the Arylhydrocarbon receptor (AhR)
    PATRICK S WONG
    Department of Environmental Toxicology and the Center for Environmental Health Sciences, University of California, One Shields Ave, Davis, CA 95616, USA
    BMC Cancer 9:234. 2009
  4. pmc Interaction of aryl hydrocarbon receptor and NF-κB subunit RelB in breast cancer is associated with interleukin-8 overexpression
    Christoph Franz Adam Vogel
    Department of Environmental Toxicology, University of California Davis, One Shields Avenue, CA 95616, USA
    Arch Biochem Biophys 512:78-86. 2011
  5. pmc A new cross-talk between the aryl hydrocarbon receptor and RelB, a member of the NF-kappaB family
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California Davis, Davis, CA 95616, USA
    Biochem Pharmacol 77:734-45. 2009
  6. ncbi Involvement of RelB in aryl hydrocarbon receptor-mediated induction of chemokines
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
    Biochem Biophys Res Commun 363:722-6. 2007
  7. pmc RelB, a new partner of aryl hydrocarbon receptor-mediated transcription
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
    Mol Endocrinol 21:2941-55. 2007
  8. pmc Pathogenesis of aryl hydrocarbon receptor-mediated development of lymphoma is associated with increased cyclooxygenase-2 expression
    Christoph F A Vogel
    Department of Environmental Toxicology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616, USA
    Am J Pathol 171:1538-48. 2007
  9. ncbi Modulation of the chemokines KC and MCP-1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice
    Christoph Franz Adam Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
    Arch Biochem Biophys 461:169-75. 2007
  10. pmc Induction of proinflammatory cytokines and C-reactive protein in human macrophage cell line U937 exposed to air pollution particulates
    Christoph Franz Adam Vogel
    Department of Environmental Toxicology, University of California, Davis, California 95616, USA
    Environ Health Perspect 113:1536-41. 2005

Collaborators

Detail Information

Publications21

  1. pmc Combustion-derived flame generated ultrafine soot generates reactive oxygen species and activates Nrf2 antioxidants differently in neonatal and adult rat lungs
    Jackie K W Chan
    Center for Health and the Environment, University of California, One Shields Ave, Davis, CA 95616, USA
    Part Fibre Toxicol 10:34. 2013
    ..5 and PM0.1 fractions and has been implicated in the generation of reactive oxygen species (ROS)...
  2. pmc Activation of inflammatory responses in human U937 macrophages by particulate matter collected from dairy farms: an in vitro expression analysis of pro-inflammatory markers
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
    Environ Health 11:17. 2012
    ....
  3. pmc Characterization of MCF mammary epithelial cells overexpressing the Arylhydrocarbon receptor (AhR)
    PATRICK S WONG
    Department of Environmental Toxicology and the Center for Environmental Health Sciences, University of California, One Shields Ave, Davis, CA 95616, USA
    BMC Cancer 9:234. 2009
    ..At the same time, the AhR serves as the mediator of the cell survival program in the absence of ER signaling...
  4. pmc Interaction of aryl hydrocarbon receptor and NF-κB subunit RelB in breast cancer is associated with interleukin-8 overexpression
    Christoph Franz Adam Vogel
    Department of Environmental Toxicology, University of California Davis, One Shields Avenue, CA 95616, USA
    Arch Biochem Biophys 512:78-86. 2011
    ..Overexpression of pro-survival factors AhR and RelB may explain the process of the development of environmentally-induced type of breast cancers...
  5. pmc A new cross-talk between the aryl hydrocarbon receptor and RelB, a member of the NF-kappaB family
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California Davis, Davis, CA 95616, USA
    Biochem Pharmacol 77:734-45. 2009
    ..Based on such information, a hypothesis has been proposed in this review that AhR together with RelB functions as a coordinator of inflammatory responses...
  6. ncbi Involvement of RelB in aryl hydrocarbon receptor-mediated induction of chemokines
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
    Biochem Biophys Res Commun 363:722-6. 2007
    ..The interaction of AhR with RelB binding on a novel type of NF-kappaB binding site represents a new regulatory function of the AhR...
  7. pmc RelB, a new partner of aryl hydrocarbon receptor-mediated transcription
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, California 95616, USA
    Mol Endocrinol 21:2941-55. 2007
    ..The interaction of RelB with AhR signaling, and AhR with NF-kappaB RelB signaling pathways represent a new mechanism of cross talk between the two transcription factors...
  8. pmc Pathogenesis of aryl hydrocarbon receptor-mediated development of lymphoma is associated with increased cyclooxygenase-2 expression
    Christoph F A Vogel
    Department of Environmental Toxicology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616, USA
    Am J Pathol 171:1538-48. 2007
    ..The results indicate that AhR activation and COX-2 overexpression likely represent a mechanism of resistance to apoptosis in lymphoma cell lines that might be relevant for the development of lymphoma in vivo...
  9. ncbi Modulation of the chemokines KC and MCP-1 by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice
    Christoph Franz Adam Vogel
    Department of Environmental Toxicology, University of California, Davis, One Shields Avenue, Davis, CA 95616, USA
    Arch Biochem Biophys 461:169-75. 2007
    ....
  10. pmc Induction of proinflammatory cytokines and C-reactive protein in human macrophage cell line U937 exposed to air pollution particulates
    Christoph Franz Adam Vogel
    Department of Environmental Toxicology, University of California, Davis, California 95616, USA
    Environ Health Perspect 113:1536-41. 2005
    ..Together, these data illustrate the interaction between particulate matter and the inflammatory response as well as the formation of cholesterol-accumulating foam cells, which are early markers of cardiovascular disease...
  11. pmc Activation of aryl hydrocarbon receptor induces vascular inflammation and promotes atherosclerosis in apolipoprotein E-/- mice
    Dalei Wu
    Department of Environmental Toxicology, University of California, Davis, CA 95616, USA
    Arterioscler Thromb Vasc Biol 31:1260-7. 2011
    ..However, the mechanisms responsible for the formation of atherosclerotic lesions mediated through AhR have not been identified...
  12. pmc AhR deficiency impairs expression of LPS-induced inflammatory genes in mice
    Dalei Wu
    Center for Health and the Environment, University of California Davis, One Shields Avenue, Davis, CA 95616, USA
    Biochem Biophys Res Commun 410:358-63. 2011
    ..The main implication of this finding is that the AhR functions in Toll-like receptor (TLR) and NF-κB signaling after activation by a classical stimulus, such as LPS...
  13. ncbi Activation of inflammatory mediators and potential role of ah-receptor ligands in foam cell formation
    Christoph F A Vogel
    Department of Environmental Toxicology and Center for Environmental Health Sciences, University of California, Davis, CA 95616, USA
    Cardiovasc Toxicol 4:363-73. 2004
    ..These findings clearly indicate that AhR ligands, like TCDD, stimulate differentiation of U937 macrophages into potentially plaque-forming foam cells...
  14. ncbi Evidence supporting the hypothesis that one of the main functions of the aryl hydrocarbon receptor is mediation of cell stress responses
    Fumio Matsumura
    Department of Environmental Toxicology, University of California, One Shields Avenue, Davis, CA 95616, USA
    Biol Chem 387:1189-94. 2006
    ..Furthermore, the process of constructing this hypothesis itself has provided us with a good opportunity to give a fresh view on the toxic action patterns of TCDD...
  15. pmc Aryl hydrocarbon receptor signaling mediates expression of indoleamine 2,3-dioxygenase
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, One Shields Avenue, Davis, CA 95616, USA
    Biochem Biophys Res Commun 375:331-5. 2008
    ....
  16. ncbi Effects of src-deficiency on the expression of in vivo toxicity of TCDD in a strain of c-src knockout mice procured through six generations of backcrossings to C57BL/6 mice
    Debra Y Dunlap
    Department of Environmental Toxicology, University of California, Davis, CA 95616, USA
    Toxicology 172:125-41. 2002
    ..These findings suggest that the absence of c-src expression indeed affects the development of selected, TCDD-induced toxic endpoints that are related to wasting syndrome...
  17. ncbi The use of c-src knockout mice for the identification of the main toxic signaling pathway of TCDD to induce wasting syndrome
    Christoph F A Vogel
    Department of Environmental Toxicology and the Center for Environmental Health Sciences, University of California, Davis, CA 95616, USA
    J Biochem Mol Toxicol 17:305-15. 2003
    ..These observations support the notion that c-Src is an important mediator of the effects of TCDD on TGFalpha, PDGF(AA), and C/EBPalpha, beta...
  18. ncbi Dioxin increases C/EBPbeta transcription by activating cAMP/protein kinase A
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, Davis, California 95616, USA
    J Biol Chem 279:8886-94. 2004
    ..Cotransfection experiments with CREB and PKA expression plasmids further supported our conclusions that the TCDD-dependent effect on C/EBPbeta transcription is mediated via PKA-dependent CREB activation...
  19. doi Development of a human adipocyte model derived from human mesenchymal stem cells (hMSC) as a tool for toxicological studies on the action of TCDD
    Wen Li
    Department of Environmental Toxicology, University of California, One Shields Avenue, Davis, CA 95616, USA
    Biol Chem 389:169-77. 2008
    ..In conclusion, hMSC-derived adipocytes appear to offer a promising human cell model suited for future toxicological studies...
  20. ncbi Interaction of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) with induced adipocyte differentiation in mouse embryonic fibroblasts (MEFs) involves tyrosine kinase c-Src
    Christoph F A Vogel
    Department of Environmental Toxicology, University of California, One Shields Avenue, Davis, CA 95616, USA
    Biochem Pharmacol 66:1231-44. 2003
    ....
  21. ncbi Studies on the cell treatment conditions to elicit lipolytic responses from 3T3-L1 adipocytes to TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin
    Wen Li
    Department of Environmental Toxicology, University of California, One Shields Avenue, Davis, California 95616, USA
    J Cell Biochem 102:389-402. 2007
    ..In conclusion, under a right condition, 3T3-L1 adipocytes were found to respond to TCDD to go through lipolysis. The early trigger of such a response appears to be activation of COX-2, which is amplified by TNFalpha...