Faculty Investigator

Cornelis Elferink, Ph.D.

Associate Professor
Department of Pharmacology & Toxicology
email: coelferi@utmb.edu

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.

Selected Publications

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.

Ge N-L, Elferink CJ.  A direct interaction between the aryl hydrocarbon receptor and retinoblastoma protein: Linking dioxin signaling to the cell cycle. J Biol Chem 273:22708-22713, 1998.

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.

Elferink CJ, 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.