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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== Materials and Methods Used ==
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==Phenotype Annotations==
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==Notes==
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==References==
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Revision as of 14:08, 15 December 2010

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

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Main Points of the Paper

Please summarize the main points of the paper.

Materials and Methods Used

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

Phenotype Annotations

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

References

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