Gary H. Perdew
About Me
I obtained a B.S. in Food Science, M.S degree in Food Biochemistry from University of Maryland and a PhD in Food Toxicology from Oregon State University. My post-doctoral experience was obtained from the University of Wisconsin at the McArdle Laboratory for Cancer Research where I studied the Aryl hydrocarbon Receptor. Next, I moved on to Purdue University in the Department of Nutrition as an assistant and associate professor, prior to moving to Penn State University in 1995 as a Professor in Veterinary and Biomedical Sciences. Throughout of career as an independent researcher I have work on the Ah receptor and the 90 kDa heat shock protein. My impact index is 65 based on 154 publications.
Department or University Committees
- Chair of the search committee for ARP director
Program or Departmental Affiliations
| BMMB Graduate Program | Molecular, Cellular, and Integrative Biosciences | Pathobiology Graduate Program |
Editorial Boards
| Ad Hoc reviewer for several NIH study sections (e.g. R35 applications) |
Centers
| Center for Molecular Toxicology and Carcinogenesis |
Research Summary
The Aryl hydrocarbon receptor (AHR) is a ligand activated transcription factor that belongs to the bHLH-PAS family. This receptor was first described to mediate the toxicity of dioxin and induce xenobiotic metabolism. We have established the biochemical pathway of AHR activation and characterized species difference in AHR mediated transcriptional activation of target genes.
The identify endogenous and bacterially generated AHR ligands have been established and this information has been utilized to examine the physiological function of the AHR. Our most recent studies are examining the function of the AHR in barrier tissues (e.g. intestine and skin) and in particular the role of the AHR in differentiation of keratinocytes and intestinal epithelial cells. We have established that activation of the AHR in barrier tissues leads to resistance to chemical challenge and offer promise in flighting various diseases. These recent discoveries have led to the pharmaceutical industry considering this receptor as a new drug target to treat various diseases and we are working with one company to test an AHR antagonist that is going into a clinical trial.
A second area of investigation is the ability of AHR activation to enhance metastatic potential and cell survival in highly aggressive tumors. We are determining whether AHR antagonist treatment will be an effective therapy for treating cancer, especially in combination with immune therapy and chemotherapy. The mechanisms that mediate this therapeutic potential are being explored.
I teach BMB 433, Biochemical and Molecular Toxicology, which explores mechanisms of toxicity upon exposure to various chemical and focus on receptor mediated carcinogenesis and toxicity.
Honors and Awards
- 2002, Penn State Faculty Scholar Medal.
- 2004 - 2006, Distinguished Professor PSU.
- 2006 - Present, Smith Endowed Professorship.
- 2009, Distinguished Alumni-Oregon State University.
- 2017, Penn State University- Howard B. Palmer Faculty Mentoring Award.
- 2019 - 2025, NIH R35 RIVER Outstanding Investigator Award- NIH grant funded for eight years.
Selected Publications
- Muku, G.E., Lahoti, T.S., Murray, I.A., Podolsky, M.A., Smith, K.J., Hubbard, T.D., Kuzu, G., Gowda, K., Amin, S.G., and Perdew, G.H. (2017) Ligand-mediated cytoplasmic retention of the Ah receptor inhibits macrophage-mediated acute inflammatory responses. Lab. Invest. 97, 1471-1487.
- Hubbard, T.D., Murray, I.A., Bisson, W.H., Sullivan, A.P., Sebastian, A., Perry, G.H., Jablonski, N.G., and Perdew, G.H. (2016) Divergent Ah receptor ligand selectivity during hominin evolution. Mol. Biol. Evol. 33, 2648-58.
- Girer, N.G., Murray, I.A., Zhang, L., Patterson, A., and Perdew, G.H. (2016) Hepatic aryl hydrocarbon receptor activity attenuates fibroblast growth factor 21 expression and modulates energy homeostasis. J. Biol. Chem. 291, 15378-87.
- Tanos, R., Patel, R.D., Murray, I.A., Smith P.B., Patterson, A.D. and Perdew, G.H. (2012) Ah receptor regulates the cholesterol biosynthetic pathway in a dioxin response element-independent manner. Hepatology 55, 1994-2004.
- DiNatale, B.C., Schroeder, J.C., Francey, L.J., Kusnadi, A. and Perdew, G.H. (2010) Mechanistic insights into the events that lead to synergistic induction of IL6 transcription upon activation of the Ah receptor and inflammatory signaling. J. Biol. Chem. 285, 24388-97.
- Beischlag, T.V. and Perdew, G.H. (2005) ER-AhR-ARNT protein-protein interactions mediate estradiol-dependent transrepression of dioxin inducible gene transcription. J. Biol. Chem. 280, 21607-21611.