Richard Ulevitch
Richard Ulevitch is professor of immunology and Chairman Emeritus of the Department of Immunology at The Scripps Research Institute.[1]
Ulevitch has an AB from Washington and Jefferson College and a PhD in Biochemistry from the University of Pennsylvania. His research attempts to understand the basic mechanisms of the innate immune response to infection. His discoveries, include the definition of the function of receptors in the innate immune system recognizing bacterial products and the discovery of a signal transduction cascade essential for an appropriate innate immune response and for regulating the production of key mediators of inflammation. He is the author of more than 200 scientific articles and his work has been among the most highly cited publications in the field of Immunology.
Ulevitch has been affiliated with multiple advisory panels including the National Institutes of Health, the American Heart Association, and the Food and Drug Administration. He is currently a scientific advisor to Aravis Ventures (Zurich, Switzerland), to 5AM Ventures (Menlo Park, CA) and a consultant to biotechnology and pharmaceutical companies. He was a founding scientific advisor to the Lombard Odier Darier Hentsch Immunology Fund (Geneva, Switzerland). Currently Dr. Ulevitch serves as Chairman of 5AM Venture's Scientific Advisory Board.
Richard is married to Susan, and is the father of David Ulevitch, the founder and CEO of OpenDNS.
Selected bibliography
- Aderem, A. and Ulevitch, R.J. Toll-like receptors in the induction of the innate immune response. Nature 406:782-787, 2000.
- Arbibe, L., Mira, J.-P., Kline, L., Godowski, P.J., Ulevitch, R.J. and Knaus, U.G. Tolllike receptor 2-mediated NF-κB activation requires a Rac1-dependent pathway. Nature Immunol. 1:533-540, 2000.
- Werts, C., Tapping, R.I., Mathison, J.C., Chuang, T.-H., Kravchenko, V. V., Saint Girons, I., Haake, D., Godowski, P.J., Hayashi, F., Ozinsky, A.,. Underhill, D., Aderem, A., Tobias, P.S. and Ulevitch, R.J. Leptospiral endotoxin activates cells via a TLR2dependent mechanism. Nature Immunol. 2:346-352, 2001.
- Ge, B., Gram, H., Di Padova, F., Huang, B., New, L., Ulevitch, R., Luo Y., and Han, J. MAP kinase-independent activation of p38a mediated by TAB 1-dependent autophosphorylation of p38a. Science 295:1291-1294, 2002.
References
- ↑ "Department of Immunology and Microbial Science". The Scripps Research Institute. Retrieved 2010-02-08.