Towards this end, we are also investigating the mechanisms used by the AraC/XylS family protein RhaS that underlie its ability to activate transcription of the appropriate genes and under the appropriate conditions. Once we identify compounds that are inhibitory, we will investigate their mechanism of action. First, we are performing a screen of a large library of small molecules for ones that specifically inhibit the activity of the AraC/XylS family protein RhaS. Towards this goal, we are currently working on two fronts. Our long-term goal is to identify small molecule inhibitors of AraC/XylS family activators. In several cases it has been shown that deletion of an AraC/XylS activator drastically reduces pathogenesis, indicating that members of this family have potential as targets for antibacterial agents. Many members of the very large AraC/XylS family of transcription activators are required for the expression of virulence factors in bacterial pathogens. We must investigate novel targets for antibacterial agents to avoid the return of commonplace deaths due to bacterial infections. The widespread availability of antibiotics since the 1940’s has dramatically reduced the number of deaths due to bacterial infections, however we are rapidly losing our advantage over our bacterial foes as antibiotic resistance becomes increasingly prevalent. Our ultimate goal is to identify small molecules that block the function of AraC family proteins and have potential as anti-bacterial agents. Many AraC family proteins are regulators of virulence factors in bacterial pathogens, therefore, we use the L-rhamnose regulators as models to understand the function of proteins in this family. coli, with a focus on the L-rhamnose catabolic genes, and the fact that the L-rhamnose regulator genes are members of the AraC family of regulatory proteins. In our lab we examine the molecular biology of gene regulation in E. My primary research interest is understanding the regulation of gene expression (especially positive regulation) at a molecular level. Regulation of bacterial transcription, Development of novel anti-bacterial agents. ![]() S., Biology, Rensselaer Polytechnic Institute, Troy, NY PhD, Microbiology, Cornell University, Ithaca, NYī. ![]() The Egan lab uses a variety of techniques including genetics, biochemistry, protein structure determination, protein-DNA interaction, and computational methods. ![]() Indeed, the lab has published a number of studies toward this goal. Understanding these mechanisms is critical to the goal of targeting activators of virulence factor expression in bacterial pathogens as a method to prevent or ameliorate disease. Research in the Egan lab focuses on the mechanisms used by bacterial transcriptional activator proteins to increase expression of specific genes under appropriate environmental conditions. She served as Associate Chair of Molecular Biosciences from 2008 through 2012, and currently serve as departmental Chairperson (since 2014). She is also an affiliate member of the Center for Computational Biology. She began her faculty position at the University of Kansas in 1994, initially in the Department of Microbiology, and following the merger of several departments, in the current Department of Molecular Biosciences. Robert Schleif at the Johns Hopkins University. in biology from Rensselaer Polytechnic Institute (1984), a PhD in microbiology from Cornell University (1991), and was a postdoctoral fellow in the lab of Dr. Regulation of bacterial transcription, Development of novel anti-bacterial agents
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