CORNELIS ELFERINK, Ph.D.
Associate Professor of Molecular Toxicology
Phone: (409) 772.9624 | Fax: (409) 772.9642 | E-mail: coelferi@utmb.edu
Websites: http://www.utmb.edu/phtox/fac/faculty.asp
“The research in my laboratory examines liver homeostasis with a particular emphasis on the molecular properties of aryl hydrocarbon receptor signaling in hepatocyte cell cycle control during liver regeneration, and in Fas ligand-induced apoptosis associated with liver injury.”
RESEARCH INTERESTS
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that, in conjunction with the AhR nuclear translocator (Arnt) protein, alters expression of numerous target genes in response to environmental stimuli. Historically, AhR studies focused on the mechanism whereby pollutants, most notably the dioxins and polychlorinated biphenyls, cause a range of adaptive and toxic endpoints. These endpoints appear to reflect disruptions in normal cell growth, cell death (apoptosis) and cell differentiation. The implication is that the AhR participates in signaling events aimed at maintaining a balance between cell growth and apoptosis. This function is central to normal development, tissue homeostasis and protection from cancer. The long-term research interest in the laboratory is to understand precisely how AhR signaling regulates cell proliferation and apoptosis in the liver, and by inference, identify the molecular basis for dioxin-induced toxicity. The laboratory uses contemporary molecular and cellular techniques as well as transgenic animal models to examine AhR function in vitro and in vivo.
PUBLICATIONS
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Mitchell, K.A., Lockhart, C.A., and Elferink, C.J. (2006). Sustained Ah receptor activity attenuates liver regeneration. Mol. Pharmacol. 70:163-170.
Szaniszlo, P., Rose, W.A., Wang, N., Reece, L.M., Tsulaia, T.V., Hanania, E.G., Elferink, C.J. and Leary,J.F. (2006). Scanning Cytometry with a LEAP: Laser-Enabled Analysis and Processing of Live Cells In Situ.
Cytometry A. 2006 Jun 28;69A(7):641-651 [Epub ahead of print].
Park, K.-T., Mitchell, K., Huang, G., and Elferink, C.J. (2005) The Ah Receptor Predisposes Hepatocytes to Fas-Mediated Apoptosis. Mol. Pharmacol. 67:612-622.
Huang, G. and Elferink, C. J. (2005). Multiple Mechanisms are Involved in Ah Receptor Mediated Cell Cycle Arrest. Mol. Pharmacol. 67:88-96.
Levine-Fridman, A., Chen, L., and Elferink, C. J. (2004). Cytochrome P4501A1 Promotes G1 Phase Cell Cycle Progression by Controlling Ah Receptor Activity. Mol. Pharmacol. 65: 461-469.
Elferink, C.J. (2003). Aryl Hydrocarbon-Mediated Cell Cycle Control. In Progress in Cell Cycle Research (eds. L. Meijer, A. Jezequel, M. Roberge) 5:261-267.
Puga, A., Xia, Y. and Elferink, C.J. (2002). Role of the Aryl Hydrocarbon Receptor in Cell Cycle Regulation. Chemico Biological Interactions 141:117-131.
Elferink, C.J. (2002). Environmental Influences on Cell Cycle Regulation. In Cellular and Molecular Toxicology. (eds. J.P. Vanden Heuvel, G.H. Perdew, W.B. Mattes, W.F. Greenlee), 14:421-443.
