red bar

Transgenic Mouse Facility
Real-time PCR Core Facility
Human Tumor Bank Core Facility
 Career Opportunities
 Funding Opportunities
 Graduate Training in Cancer
   Cancer Cell Biology Track
   SCCCB Predoctoral Fellowship
   Cancer Center Training Grant
In the News
 Related Links
 Site Index
 Software - Molecular Biology Tools
 UTMB Cancer Center
 UTMB Home Page

Faculty Investigator

Dr. Cornelis Elferink

Cornelis Elferink, Ph.D.

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

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. Elferink Lab

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.

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, 2001.

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

red bar
This site is published by John Helms for the Sealy Center for Cancer Cell Biology.
Copyright © 2003
The University of Texas Medical Branch. Please review our Privacy Policy and Internet Guidelines.
Last reviewed: November 5, 2008.