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Academic Background

Timothy Kowalik received his B.S. degree in Biology and Mathematics from Belmont Abbey College in 1982. He received his M.S. (1986) and his Ph.D. (1989) in Molecular Biology and Virology from Utah State University. Dr. Kowalik did postdoctoral research on virus-cell interactions from 1990-1993 at the Lineberger Cancer Center of the University of North Carolina. From 1993-1996, he continued his postdoctoral studies in the Department of Genetics at Duke University Medical Center where he analyzed the relationship between the cell cycle and apoptosis. During his postdoctoral training, Dr. Kowalik was a Fellow of the Damon Runyon-Walter Winchell Cancer Research Fund and a Leukemia Society of America Special Fellow. In 1996, Dr. Kowalik joined the Department of Molecular Genetics and Microbiology at the University of Massachusetts Medical School where he is an associate professor.

Cell activation and DNA viruses

Photo: Timothy 
F. KowalikResearch in my laboratory centers around the regulation of cellular proliferation control especially from the perspective of an infecting virus. To maximize yields, small DNA tumor viruses encode activities which trick infected cells into proliferative states. This is often achieved by subverting normal homeostatic controls resulting in infected cells progressing into S phase. For small DNA viruses, this entails inactivating the Rb and p53 tumor suppressors. Rb inactivation results in the activation of the E2F transcription factor family which induces expression of genes involved in nucleotide and DNA biosynthesis. Genetic and biochemical studies have demonstrated that Rb inactivation and induction of E2F transcriptional activity normally occur in late G1 and are central to the progression of cells through G1 and into S phase.

Using recombinant adenovirus technology, we are presently examining the paradoxical relationship between growth activation by E2F1 overexpression and the resultant p53-dependent apoptotic cell death. We are also studying the consequences of Rb and p53 targeting by large DNA tumor viruses including members of the herpesvirus family.


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