| pubmed-article:15036322 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15036322 | lifeskim:mentions | umls-concept:C0003232 | lld:lifeskim |
| pubmed-article:15036322 | lifeskim:mentions | umls-concept:C0521009 | lld:lifeskim |
| pubmed-article:15036322 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:15036322 | lifeskim:mentions | umls-concept:C1521840 | lld:lifeskim |
| pubmed-article:15036322 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15036322 | pubmed:dateCreated | 2004-3-23 | lld:pubmed |
| pubmed-article:15036322 | pubmed:abstractText | Growing experimental evidence has revealed the existence of programmed cell death (PCD) systems in bacteria. Among these is the mazEF system, which is a regulable suicide module located on the chromosome of E. coli and of some other bacteria, including pathogens. Several well-known antibiotics have recently been found to cause cell death in E. coli by indirectly activating this built-in suicide module. These antibiotics belong to two groups: (i) inhibitors of transcription and/or translation; and (ii) inhibitors of folic acid metabolism resulting in thymine starvation. These data, together with the recent elucidation of the crystal structure of mazEF-directed components, hold promise for a rational chemical design of a new class of antibiotics that directly activate chromosomal suicide modules by interacting with their components. Because multi-drug resistance among bacterial pathogens is becoming more widespread, the results obtained might be useful as a basis for producing alternative drugs. | lld:pubmed |
| pubmed-article:15036322 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:15036322 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15036322 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15036322 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:15036322 | pubmed:issn | 0966-842X | lld:pubmed |
| pubmed-article:15036322 | pubmed:author | pubmed-author:Engelberg-Kul... | lld:pubmed |
| pubmed-article:15036322 | pubmed:author | pubmed-author:SatBoazB | lld:pubmed |
| pubmed-article:15036322 | pubmed:author | pubmed-author:RechesMyriamM | lld:pubmed |
| pubmed-article:15036322 | pubmed:author | pubmed-author:HazanRonenR | lld:pubmed |
| pubmed-article:15036322 | pubmed:author | pubmed-author:AmitaiShaharS | lld:pubmed |
| pubmed-article:15036322 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15036322 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:15036322 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15036322 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15036322 | pubmed:pagination | 66-71 | lld:pubmed |
| pubmed-article:15036322 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:15036322 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15036322 | pubmed:articleTitle | Bacterial programmed cell death systems as targets for antibiotics. | lld:pubmed |
| pubmed-article:15036322 | pubmed:affiliation | Department of Molecular Biology, The Hebrew University-Hadassah Medical School, Jerusalem 91120, Israel. hanita@cc.huji.ac.il | lld:pubmed |
| pubmed-article:15036322 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15036322 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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