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  ε/ζ systems: their role in resistance, virulence, and their potential for antibiotic development

Mutschler, H., & Meinhart, A. (2011). ε/ζ systems: their role in resistance, virulence, and their potential for antibiotic development. Journal of Molecular Medicine, 89(12), 1183-1194. doi:10.1007/s00109-011-0797-4.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0024-1E99-8 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0024-1E9A-6
Genre: Journal Article
Alternative Title : ε/ζ systems: their role in resistance, virulence, and their potential for antibiotic development

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JMolMedicine_89_2011_1183.pdf (Any fulltext), 982KB
 
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 Creators:
Mutschler, Hannes1, Author              
Meinhart, Anton1, Author              
Affiliations:
1Department of Biomolecular Mechanisms, Max Planck Institute for Medical Research, Max Planck Society, ou_1497700              

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Free keywords: Antimicrobial peptides . Biochemistry. Cell death . Drug development . Drug resistance . Infectiology
 Abstract: Cell death in bacteria can be triggered by activation of self−inflicted molecular mechanisms. Pathogenic bacteria often make use of suicide mechanisms in which the death of individual cells benefits survival of the population. Important elements for programmed cell death in bacteria are proteinaceous toxin−antitoxin systems. While the toxin generally resides dormant in the bacterial cytosol in complex with its antitoxin, conditions such as impaired de novo synthesis of the antitoxin or nutritional stress lead to antitoxin degradation and toxin activation. A widespread toxin−antitoxin family consists of the ε/ζ systems, which are distributed over plasmids and chromosomes of various pathogenic bacteria. In its inactive state, the bacteriotoxic ζ toxin protein is inhibited by its cognate antitoxin ε. Upon degradation of ε, the ζ toxin is released allowing this enzyme to poison bacterial cell wall synthesis, which eventually triggers autolysis. ε/ζ systems ensure stable plasmid inheritance by inducing death in plasmid−deprived offspring cells. In contrast, chromosomally encoded ε/ζ systems were reported to contribute to virulence of pathogenic bacteria, possibly by inducing autolysis in individual cells under stressful conditions. The capability of toxin−antitoxin systems to kill bacteria has made them potential targets for new therapeutic compounds. Toxin activation could be hijacked to induce suicide of bacteria. Likewise, the unique mechanism of ζ toxins could serve as template for new drugs. Contrarily, inhibition of virulence−associated ζ toxins might attenuate infections. Here we provide an overview of ε/ζ toxin−antitoxin family and its potential role in the development of new therapeutic approaches in microbial defense

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Language(s): eng - English
 Dates: 2011-07-192011-06-202011-07-222011-08-062011-12-01
 Publication Status: Published in print
 Pages: 12
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 664490
DOI: 10.1007/s00109-011-0797-4
Other: 7688
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Title: Journal of Molecular Medicine
Source Genre: Journal
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Publ. Info: Berlin : Springer
Pages: - Volume / Issue: 89 (12) Sequence Number: - Start / End Page: 1183 - 1194 Identifier: ISSN: 0946-2716
CoNE: https://pure.mpg.de/cone/journals/resource/954926989131_1