Philip E. Auron, Ph.D.Professor
Bayer School of Natural and Environmental Sciences
232A Mellon Hall
Education:PostGrad, Molecular Biology, Massachusetts Institute of Technology, 1982
Ph.D., Biochemistry, Pennslvania State University, 1980
B.S., Biology, Wilkes College, 1974
Dr. Auron received his Ph.D. in Biochemistry from the Pennsylvania State University in 1980, studying prokaryotic ribosome structure and function. He then conducted postdoctoral studies at The Massachusetts Institute of Technology using chemical and enzymatic techniques in concert with computer algorithmic model building and X-ray crystal structure data to predict the structure of small (tRNA) and large (rRNA and mRNA) ribonucleic acid molecules in solution.
In 1983 Dr. Auron accepted a faculty position as an Assistant Professor at Tufts University School of Medicine in Boston, while maintaining a joint visiting faculty position and laboratory at MIT in the joint Harvard-MIT division of Health Sciences and Technology. It was at this time that he initiated seminal studies leading to the characterization of interleukin 1 beta and its gene structure and regulation.
In 1989, Dr. Auron joined the faculty in the Department of Pathology at Harvard Medical School and was promoted to Associate Professor in 1993. Dr. Auron joined the Department of Molecular Genetics and Biochemistry at the University of Pittsburgh School of Medicine in 2002 and accepted the chairmanship of the Department of Biological Sciences at Duquesne in 2006, a position that he held until 2010.
Dr. Auron's interests in the relationship between molecular structure and function have guided his work. Most studies have focused on mechanistic approaches that often rely upon correlation with known high-resolution structures and molecular model building.
Dr. Auron has also contributed to the bioinformatics field, having published several papers dealing with nucleic acid analysis software and hardware. Two commercial software packages aimed at molecular biology users have resulted from his efforts.
In March, 1982, Dr. Auron was a member of the group that submitted the original contract application proposal for the GenBank database which resulted in the establishment of that famous repository. Finally, Dr. Auron was involved in high-profile landmark litigation in which he defended the sanctity of confidentiality during the peer review process (Science 273:1162-4, 1996; Nature 384:1-4, 1996; Biotechnology 14:14, 1996; Nature Biotechnology 14:275-9, 1996; The Washington Post April 19, 1996, p.D1); and JAMA - Third International Congress on Biomedical Peer Review and Global Communications Sept. 18-20, 1997.
The research focuses on molecular mechanisms of cytokine gene regulation. One of these cytokines is interleukin 1 (IL-1) which influences genes expressing various proteins that can modulate the level of acute and chronic inflammation and thus mediate subsequent fever and tissue destruction. In 1984, Dr. Auron was involved in the original cloning and characterization of IL-1beta cDNA. This was followed by the isolation and sequencing of the corresponding IL1B gene locus. The induced IL1B gene product is involved in inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, arteriosclerosis, bacterial sepsis and infection by certain viruses.
The laboratory has placed emphasis on the detailed molecular processes and structures involved both in receptor signal transduction and gene transcription in normal cells and those expressing proinflammatory proteins derived from cytomegalovirus infection. Attention has also been paid to cell-type-specific expression. As a result, Dr. Auron and his collaborators have determined that the monomyeloid-specific ETS domain transcription factor, Spi-1/PU.1, is required for vigorous expression of the IL1B gene. They have also determined that physical interaction between Spi-1 and GATA-family proteins is responsible for a mutual inhibition that is critical for stem cell commitment to erythroid vs. mono-myeloid lineage development in hematopoiesis. Spi-1, which is essential for monocyte and osteoclast development, binds to the IL1B gene and couples the gene induction signal, found in a distinct location approximately 3kbp upstream from the transcription start site, directly to the general transcription machinery. The Spi-1/PU.1 factor is also targeted during human cytomegalovirus (HCMV) infection and mediates viral-induction of IL1B by eliminating the requirement for the exogenous activation signal via one specific HCMV protein (IE2, immediate early protein 2). Research focusing on receptor signal transduction has resulted in the discovery that the IL-1 receptor-activated intracellular signal transducer called TRAF6 functions through at least two distinct pathways that result in differential activation of Rel/NF-kappaB transcription factor family members. This may be responsible for some of the known subtleties of the inflammatory response.
For more information regarding Auron Lab research, see: http://www.scienceresearch.duq.edu/bio/biofac/pauron.
As of 12-1-11, Dr. Auron has 95 publications reflected by statistics that include 6410 total citations for 81 of these articles, reflecting an average of 79 citations per publication and an h-index of 42. One research paper (Auron PE, et al., 1984. Nucleotide sequence of human monocyte interleukin-1 precursor cDNA. Proc. Natl. Acad. Sci., USA 81:7907-7911.) garnered 1048 citations and has been awarded both Science Citation Classic and Pillar of Immunology designations, respectively, by the Institute for Scientific Information and the American Association of Immunologists. In addition, P.E. Auron appears as first or senior author on 52 of the 95 references.
Many of Dr. Auron's publications can be accessed through the NIH Medline database: http://www.ncbi.nlm.nih.gov/pubmed?term=auron%20p.