James Olesen
Assistant Professor of Biology
Education
Bowling Green State University, Ph.D.,1994
The Ohio State University, M.S.,1987
Bowling Green State University, B.S. ,1983
Research Interests
My general interests are in molecular and cancer biology.
Specific Goal: Understanding how ectopic expression of the transcription factor, TAL-1 (see Fig. 1), contributes to leukemogenesis. Through ill-defined mechanisms, TAL-1 seems to play a significant role in the progression of T-cell acute lymphoblastic leukemia. It is thought that important cellular processes such as cell cycle control, cell signaling and apoptosis (see Fig. 2) are influenced by this mis-expressed protein. Through investigating potential targets of TAL-1, it is hoped that a better picture of how TAL-1 influences apoptotic resistance and cell survival will be realized. In the end, this type of research will hopefully guide the future development of better, more targeted therapies to treat T-ALL at the molecular level.
In our research, we:
- Assess protein expression in isolated cellular extracts via Western blotting.
- Characterize intracellular protein expression levels though the use of flow cytometry.
- Utilize immunofluorescence and confocal microscopy to investigate the localization of various proteins within cells (see Fig. 3).
- Study the apoptotic response in the malignant Jurkat cell line as measured by caspase activity and TUNEL assays.
Recent Publications:
Bombuwala, K., Kinstle, t., Popik, V., Uppal, S., Olesen, J.B., Vina, J. and Heckman, C.A. (2006). Colchitaxel, A Coupled Compound Made from Microtubule Inhibitors Colchcine and Paclitaxel. Beilstein Journal of Organic Chemistry 2:13-22.
Olesen, J.B. and Gough, E. (2006). Optimization of Transfection Conditions for the Human HL-60 Promyelocytic Leukemic T-Cell Line Using FuGene HD Transfection Reagent. Biochemica, 3:24-25.
Lucas, B. and Olesen, J.B. Ectopic expression of TAL-1 increases resistance to TNFα-induced apoptosis in Jurkat cells via changes in the NF-κB signaling pathway. In preparation.