Probing the Binding Site in the Antibiotic Resistance Enzyme, AmpC Beta-lactamase

Presentation Type

Poster/Portfolio

Presenter Major(s)

Chemistry

Mentor Information

Brad Wallar

Department

Chemistry

Location

Henry Hall Atrium 42

Start Date

10-4-2013 1:00 PM

End Date

10-4-2013 2:00 PM

Keywords

Health, Life Science, Physical Science

Abstract

Beta-lactam drugs, such as penicillins and cephalosporins, are widely used to treat bacterial infections, but resistance to these drugs is increasingly becoming a problem. One of the main causes of resistance to these beta-lactam drugs is the bacterial production of beta-lactamase enzymes, such as AmpC. These enzymes are capable of breaking down the drug within their active sites, rendering the antibiotic unable to harm the bacteria. The exact roles that the active site amino acid residues play in the recognition and breakdown of the drug are not fully understood. Here, we investigate the role of the active site residue asparagine-152 (Asn152) in AmpC by mutating it to a glycine, serine, or threonine residue and examining the effect that these mutations have on kinetic and structural properties. Uncovering the specific role of Asn152 in the function of AmpC will be useful in the development of inhibitors to these enzymes in order to combat bacterial resistance.

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Apr 10th, 1:00 PM Apr 10th, 2:00 PM

Probing the Binding Site in the Antibiotic Resistance Enzyme, AmpC Beta-lactamase

Henry Hall Atrium 42

Beta-lactam drugs, such as penicillins and cephalosporins, are widely used to treat bacterial infections, but resistance to these drugs is increasingly becoming a problem. One of the main causes of resistance to these beta-lactam drugs is the bacterial production of beta-lactamase enzymes, such as AmpC. These enzymes are capable of breaking down the drug within their active sites, rendering the antibiotic unable to harm the bacteria. The exact roles that the active site amino acid residues play in the recognition and breakdown of the drug are not fully understood. Here, we investigate the role of the active site residue asparagine-152 (Asn152) in AmpC by mutating it to a glycine, serine, or threonine residue and examining the effect that these mutations have on kinetic and structural properties. Uncovering the specific role of Asn152 in the function of AmpC will be useful in the development of inhibitors to these enzymes in order to combat bacterial resistance.