Researchers at the Antimicrobial Discovery Center have recently discovered that the acyldepsipeptide antibiotic, ADEP4, stimulates the proteolytic mechanism of ClpP protease and cells, killing persister cells by forcing them to degrade a range of cellular proteins.
The dual nature of bacterial drug reactions raises concerns about the ability of today's antibiotics to cope with future infections. Some bacteria form genetic resistance, while others become tolerant by forming a dormant cell called "persister" in which the enzyme target of the antibiotic is inactivated. Survival in existence.
The researchers conducted research to search for drugs that could kill persister cells by destroying these energy-limited intracellular targets. They found that the acyldepsipeptide antibiotic ADEP4 stimulates the proteolytic mechanism of ClpP protease and cells, killing them by forcing the persister cells to degrade a range of cellular proteins. This is a potentially important result, suggesting that combining drugs such as ADEP4 with traditional antibiotics may provide a new and reliable strategy for the control of chronic infections.
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