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Insect defenses point the way to defeating bacterial antibiotic resistance

r which they were designed. Heat shock proteins help repair the problems, correcting the shapes of the proteins and restoring them to functionality.

The mechanism by which the sap-sucking insect's antimicrobial molecule kills bacteria, then, is to disrupt the bacterial heat-shock protein repair system. Importantly, this insect peptide does not bind to the human equivalent of the DnaK receptor, known as Hsp70, greatly enhancing its pharmaceutical potential in humans. If the peptide bound to the human Hsp70 receptor, it and related compounds might pose a danger to human cells.

With the receptor now identified, scientists might be able to develop new drug compounds with improved characteristics that act on the same site. The new compounds might be more easily synthesized than the naturally occurring one, for example, or show greater stability in mammalian systems. They might also be tailored to target specific bacterial or fungal strains with heightened effectiveness.


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Contact: Franklin Hoke
hoke@wistar.upenn.edu
215-898-3716
The Wistar Institute
22-Oct-2000


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