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. 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.