Department of Pharmacology & Toxicology
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, 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.
Reiners JJ Jr,
Jones CJL, Hong N, Clift R, Elferink CJ. Down regulation of aryl hydro-carbon receptor
function by expression of h-ras oncogenes. Mol Carcinogenesis 19:91-100, 1997.
Elferink CJ. A direct interaction between the aryl hydrocarbon receptor and
retinoblastoma protein: Linking dioxin signaling to the cell cycle. J Biol Chem
Santini R, Myrand S, Elferink CJ, Reiners JJ Jr. Regulation of Cyp1a1 induction by
dioxin as a function of cell cycle phase. J Pharmacol Exp Therapeutics 299:718-728, 2001.
Ge N-L, Levine A. Maximal aryl hydrocarbon receptor activity depends on an interaction
with the retinoblastoma protein. Mol Pharmacol 59:664-673, 2001.
Hines RN, Luo Z, Cresteil T, Ding X, Prough RA, Fitzpatrick JL, Ripp SL, Falkner KC, Ge N-L,
Levine A, Elferink, CJ Molecular regulation of genes encoding xenobiotic
metabolizing enzymes: Mechanisms involving endogenous factors. Drug
Metabolism and Disposition 29:623-633, 2001.
Stracevic SL, Elferink CJ, Novak RF. Progressive resistance to apoptosis in
a cell lineage model of human proliferative breast disease. J Natl Cancer Inst 93(10):776-82,
Puga A, Xia Y, Elferink CJ. Role of the aryl hydrocarbon receptor in cell cycle
regulation. Chemico Biological Interactions 141:117-131, 2002.
Elferink CJ. Aryl
hydrocarbon-mediated cell cycle control. In Progress in Cell Cycle Research (eds. L.
Meijer, A. Jezequel, M. Roberge) 5:261-267, 2003.
Levine-Fridman A, Chen L, Elferink CJ. Cytochrome P4501A1 promotes G1 phase cell
cycle progression by controlling Ah receptor activity. Mol Pharmacol 65:461-469, 2004.
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