Difference between revisions of "PMID:20440275"

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{|  id="N4d09121059127"  class=" tableEdit PMID_info_table" 
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!align=left  |Citation
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'''Kohanski, MA, Dwyer, DJ and Collins, JJ'''  (2010) How antibiotics kill bacteria: from targets to networks.''Nat. Rev. Microbiol.'' '''8''':423-35
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!align=left  |Abstract
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Antibiotic drug-target interactions, and their respective direct effects, are generally well characterized. By contrast, the bacterial responses to antibiotic drug treatments that contribute to cell death are not as well understood and have proven to be complex as they involve many genetic and biochemical pathways. In this Review, we discuss the multilayered effects of drug-target interactions, including the essential cellular processes that are inhibited by bactericidal antibiotics and the associated cellular response mechanisms that contribute to killing. We also discuss new insights into these mechanisms that have been revealed through the study of biological networks, and describe how these insights, together with related developments in synthetic biology, could be exploited to create new antibacterial therapies.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=20440275 PubMed]
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Online version:[http://dx.doi.org/10.1038/nrmicro2333 10.1038/nrmicro2333]
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!align=left  |Keywords
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Anti-Bacterial Agents; Bacteria; Cell Wall; DNA Replication; Drug Discovery; Nucleic Acid Synthesis Inhibitors; Quinolones; RNA; Rifamycins
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==Main Points of the Paper ==
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{{LitSignificance}}
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This review on antibiotic mechanisms argues that in many cases cell killing by antibiotics with diverse targets is due to a common indirect mechanism involving induction of oxidative stress leading to hydroxyl radical production.  See Figure 2.
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== Materials and Methods Used ==
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{{LitMaterials}}
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==Phenotype Annotations==
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{|  id="I4d09121068b61"  class=" tableEdit PMID_Phenotype_table" 
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!|Species!!Taxon ID!!Strain!!Gene (if known)!!OMP!!Phenotype!!Details!!Evidence!!Notes
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Inhibition of DNA replication
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Inhibition of RNA synthesis
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* rifampicin
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* streptolydigin
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* amanitin (eukaryotes)
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Inhibition of cell wall synthesis
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Sensitivity to
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Inhibition of cell wall synthesis resulting in lysis
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Sensitivity to
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Sensitivity to
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Induction of hydroxyl radical production
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* uncouplers
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* pore-formers
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==Notes==
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==References==
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{{RefHelp}}
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<references/>
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[[Category:Publication]]
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[[Category:To Be Converted]]

Latest revision as of 12:09, 22 June 2011

Citation

Kohanski, MA, Dwyer, DJ and Collins, JJ (2010) How antibiotics kill bacteria: from targets to networks.Nat. Rev. Microbiol. 8:423-35

Abstract

Antibiotic drug-target interactions, and their respective direct effects, are generally well characterized. By contrast, the bacterial responses to antibiotic drug treatments that contribute to cell death are not as well understood and have proven to be complex as they involve many genetic and biochemical pathways. In this Review, we discuss the multilayered effects of drug-target interactions, including the essential cellular processes that are inhibited by bactericidal antibiotics and the associated cellular response mechanisms that contribute to killing. We also discuss new insights into these mechanisms that have been revealed through the study of biological networks, and describe how these insights, together with related developments in synthetic biology, could be exploited to create new antibacterial therapies.

Links

PubMed Online version:10.1038/nrmicro2333

Keywords

Anti-Bacterial Agents; Bacteria; Cell Wall; DNA Replication; Drug Discovery; Nucleic Acid Synthesis Inhibitors; Quinolones; RNA; Rifamycins

edit table

Main Points of the Paper

Please summarize the main points of the paper.

This review on antibiotic mechanisms argues that in many cases cell killing by antibiotics with diverse targets is due to a common indirect mechanism involving induction of oxidative stress leading to hydroxyl radical production. See Figure 2.

Materials and Methods Used

Please list the materials and methods used in this paper (strains, plasmids, antibodies, etc).

Phenotype Annotations

See Help:AnnotationTable for details on how to edit this table.
<protect>

Species Taxon ID Strain Gene (if known) OMP Phenotype Details Evidence Notes

Sensitivity to

Inhibition of DNA replication

Sensitivity to

topoisomerase-catalysed DNA strand breakage

Sensitivity to

Inhibition of RNA synthesis

  • rifampicin
  • streptolydigin
  • amanitin (eukaryotes)

Sensitivity to

Inhibition of cell wall synthesis

Sensitivity to

Inhibition of cell wall synthesis resulting in lysis

Sensitivity to

Inhibition of protein synthesis

Sensitivity to

Increased protein mistranslation

Sensitivity to

Induction of hydroxyl radical production

Sensitivity to

Loss of membrane potential

  • uncouplers
  • pore-formers
edit table

</protect>

Notes

References

See Help:References for how to manage references in omp dev.

Retrieved from "http://bcbp-ftq4xm2.biobio.tamu.edu/omp/dev/index.php?title=PMID:20440275&oldid=5160"