Human African Trypanosomiasis (HAT) is a neglected tropical disease endemic to rural communities in sub-Saharan Africa caused by the protozoan, Trypanosoma brucei. Current drugs are more than 20 years old, highly toxic, and difficult to administer. The best lead drugs to treat HAT will target essential cellular processes in T. brucei that are deeply diverged from the vertebrate host. Unfortunately, studying deeply diverged processes is difficult since, by definition, there is little homology to well studied systems (e.g. vertebrates). This means that using homology-based strategies to identify and study essential proteins in T. brucei is not practical. The Kojo Mensa-Wilmot lab advocates a chemical biology approach to identify and study T. brucei proteins and their cellular processes. This approach involves the screening of small molecules that elicit a phenotypic change in the parasite. The identified small molecules are then used as tools in chemical proteomics strategies to identify their potential targets. The identified targets are then verified as modulators of the observed drug treatment phenotypes by molecular based cell biology studies (RNAi knockdown). This scheme is currently being applied to study cell cycle (Sarah M. Thomas and Catherine E. Sullenberger), transferrin endocytosis (Paul J. Guyett), cell morphology/polarity (Ranjan K. Behera), as well as organelle replication and morphogenesis. An intriguing outcome of these studies includes the identification and optimization of new lead drugs to treat HAT.

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UGA institutions associated with the research project: 
CTEGD
Center for Drug Discovery (Pharmaceutical and Biomedical Sciences)
Interdisciplinary Life Sciences
Department of Biochemistry and Molecular Biology