Organisms which cause chronic disease have a unique relationship with their environment. Whether a parasite, such as an African trypanosome, or an opportunistic pathogen, like Candida albicans , each must evolve strategies for their persistence, transmission and replication in either an immunocompetent or immunocompromised host. Moreover, the pattern of gene expression can vary significantly in the different microenvironments provided by specific tissue and organ systems. Our laboratory is interested in discovering and investigating the underlying mechanisms of pathogenesis for both protozoan and fungal pathogens at the molecular and genetic level. Most recently we have been using the genomic sequence derived for the fungus, Candida albicans to develop DNA microarrays which will allow genome-wide expression analysis. For the first time we are able to look at the interrelationships between genes and biological pathways and to determine the patterns of gene expression in different disease presentations, at lesions in different host tissues and to compare the human disease with that replicated in relevant animal models. This technology is being applied to the characterization of virulence factors and mechanisms of pathogenesis for this opportunistic pathogen.
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Dungan, J, Watkins, K, and Agabian, N. Evidence for the presence of a small U5- like RNA in active trans-spliceosomes of Trypanosoma brucei. Embo J., 15 (1996): 4016-4029.
Newport, G and Agabian, N. KEX2 influences Candida albicans proteinase secretion and hyphal formation. J. Biol. Chem. 272(46) (1997): 28954-28961.
Byington, CL, Dunbrack, Jr., RL, Whitby, FG, Cohen, FE, and Agabian, N. Entamoeba histolytica: Computer-Assisted Modeling of Phosphofructokinase for the Prediction of Broad Spectrum Antiparasitic Agents. Expt'l. Parasitol. 87(3) (1997): 1 94-202.
information last updated February 2003 |