pubmed-article:17402841 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17402841 | lifeskim:mentions | umls-concept:C0004623 | lld:lifeskim |
pubmed-article:17402841 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
pubmed-article:17402841 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
pubmed-article:17402841 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:17402841 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
pubmed-article:17402841 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
pubmed-article:17402841 | lifeskim:mentions | umls-concept:C1292724 | lld:lifeskim |
pubmed-article:17402841 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:17402841 | pubmed:dateCreated | 2007-4-3 | lld:pubmed |
pubmed-article:17402841 | pubmed:abstractText | The growing challenge of antimicrobial resistance and the paucity of novel antibiotics underscore the importance of developing novel therapeutics. Bacterial cell-to-cell signaling constitutes a novel drug target. Quorum sensing (QS) is a cell-to-cell signaling mechanism that refers to the ability of bacteria to respond to chemical hormone-like molecules called autoinducers. QS is responsible for controlling a plethora of virulence genes in several bacterial pathogens. Antagonists to autoinducers will intercept bacterial intercellular communication, hindering their ability to act in a coordinated manner to express virulence traits. Moreover, since QS is not involved directly in essential processes, such as bacterial growth, one can reason that inhibition of QS will not yield a selective pressure for the development of resistance. | lld:pubmed |
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pubmed-article:17402841 | pubmed:language | eng | lld:pubmed |
pubmed-article:17402841 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17402841 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:17402841 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17402841 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17402841 | pubmed:month | Apr | lld:pubmed |
pubmed-article:17402841 | pubmed:issn | 1744-8336 | lld:pubmed |
pubmed-article:17402841 | pubmed:author | pubmed-author:SperandioVane... | lld:pubmed |
pubmed-article:17402841 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:17402841 | pubmed:volume | 5 | lld:pubmed |
pubmed-article:17402841 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17402841 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17402841 | pubmed:pagination | 271-6 | lld:pubmed |
pubmed-article:17402841 | pubmed:dateRevised | 2010-10-6 | lld:pubmed |
pubmed-article:17402841 | pubmed:meshHeading | pubmed-meshheading:17402841... | lld:pubmed |
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pubmed-article:17402841 | pubmed:meshHeading | pubmed-meshheading:17402841... | lld:pubmed |
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pubmed-article:17402841 | pubmed:meshHeading | pubmed-meshheading:17402841... | lld:pubmed |
pubmed-article:17402841 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:17402841 | pubmed:articleTitle | Novel approaches to bacterial infection therapy by interfering with bacteria-to-bacteria signaling. | lld:pubmed |
pubmed-article:17402841 | pubmed:affiliation | University of Texas Southwestern Medical Center, Dept of Microbiology, 5325 Harry Hines Blvd, Dallas, TX 75390-9048, USA. vanessa.sperandio@utsouthwestern.edu | lld:pubmed |
pubmed-article:17402841 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:17402841 | pubmed:publicationType | Review | lld:pubmed |
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