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Training
- B.Sc., 1978: Purdue University, West Lafayette, IN
- M.Sc. 1980: University of TexasSchool of Public Health
- Ph.D., 1985: University of North Carolina-Chapel Hill
- Post Doctoral, 1985-1987: University of Southern California
- Post Doctoral, 1987-1988: Indiana University School of Medicine, Indianapolis, IN
Positions
- Professor, 2000-present: Department Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN
- Member, 2000-present: Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN
- Primary Appointment, 1995-present: Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN
- Full Member, 1994-present: Indiana University Graduate School Faculty, Indiana University School of Medicine, Indianapolis, IN
- Associate Professor, 1993-present: Departments of Medicine and Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN
- Associate Professor, 1993-1999: Department Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN
- Associate Member, 1990-1994: Indiana University Graduate School Faculty, Indiana University School of Medicine, Indianapolis, IN
- Assistant Professor, 1989-1993: Department of Biochemistry & Molecular Biology, Indiana University School of Medicine, Indianapolis, IN
- Assistant Professor of Medicine, 1988-1993: Indiana University School of Medicine, Indianapolis, IN
- Assistant Member, 1988-1993: Walther Oncology Center, Indiana University School of Medicine, Indianapolis, IN
 Summary of the focus of the research of Dr. Harrington:
We are interested determining how the innate immune response is regulated. The innate immune response is an important line of defense against pathogenic agents and is also an integral component of the wound repair process. In vivo, the cytokines, tumor necrosis factor-a (TNFa) and interleukin-1 (IL-1) activate the innate immune response by increasing NF-kB dependent expression of genes. We recently identified a novel serine/threonine protein kinase, mouse Pelle-like kinase (mPLK). mPLK shares a high degree of sequence similarity with the Drosophila Pelle protein kinase. In Drosophila, Pelle is in a signaling pathway upstream of Dorsal, a Drosophila NF-kB equivalent and is involved in the host immune response. Recent studies on mPLK have revealed that mPLK is a component of a TNFa signaling pathway that results in activation of NF-kB dependent genes. Ongoing studies in the laboratory are aimed at elucidating the mechanism(s) through which TNFa activates mPLK and how mPLK mediates induction of NF-kB activity. More recently, we have identifed a second novel protein kinase, that shares limited homology with mPLK. In contrast to the anti-apoptotic response detected with mPLK, this novel kinase initiates apoptosis. Ongoing studies in the laboratory are aimed at identifying upstream regulators of RIP3 and defining the mechanism through which RIP3 induces apoptosis. An intriguing aspect of the Drosophila Pelle protein is the requirement for the Pelle protein during early embryogenesis in addition to its role in the adult immune response. A long term goal ofour laboratory is to elucidate whether mPLK, and potentially RIP3, play a role in early mammalian development.
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