- Associate Professor, Faculty of Health Sciences
Office: BLU 11512
Personal site: http://www.sfu.ca/~tvb/
- BS, Honors Pharmacology, University of Toronto
- MSc, Pharmacology, University of Toronto
- PhD, Department of Pharmacology, University of Toronto
- Postdoctoral Research, University of California/Los Angeles
Dr. Beischlag received his PhD from the University of Toronto in 1996. There he cloned and studied the transcriptional regulation of dopamine receptor genes. Following his PhD, Dr. Beischlag’s post-doctoral research began at the University of California/Los Angeles where he studied and characterized the molecular determinants of aryl hydrocarbon receptor-mediated gene transcription. He continued this work at the University of California/San Diego. In 2004, Dr. Beischlag joined the Center for Molecular Toxicology and Carcinogenesis at Pennsylvania State University as an assistant research professor. Dr. Beischlag joined the Faculty of Health Sciences in 2007.
Dr. Beischlag is actively seeking M.Sc. and Ph.D. level graduate students for his lab. Interested candidates should apply directly to Dr. Beischlag at: email@example.com
More information about the Beischlag Lab.
Research in my laboratory is focused on the molecular determinants of biological signaling pathways involved in chemical carcinogenesis and related toxicities. In particular, we are interested in how dioxins, poly-chlorinated biphenyls (PCB’s), and related compounds activate the aryl hydrocarbon or dioxin receptor (AHR) and how this system interacts with other signaling systems. The AHR mediates most, if not all of the toxic effects of these ubiquitous environmental pollutants. Upon activation, AHR binds DNA and initiates the transcription of a battery of target genes including those that encode for xenobiotic metabolizing enzymes. In addition, the AHR interacts with other transcription factors, including nuclear hormone receptors, to modulate and/or disrupt their activity. It is our goal to elucidate the molecular events underlying AHR-mediated toxicities as well as normal AHR physiology.