pubmed-article:12234837 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C0242767 | lld:lifeskim |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C0038172 | lld:lifeskim |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C0079830 | lld:lifeskim |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C1186763 | lld:lifeskim |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C0030958 | lld:lifeskim |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C0596260 | lld:lifeskim |
pubmed-article:12234837 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
pubmed-article:12234837 | pubmed:issue | 10 | lld:pubmed |
pubmed-article:12234837 | pubmed:dateCreated | 2002-9-17 | lld:pubmed |
pubmed-article:12234837 | pubmed:abstractText | A mecA-containing Staphylococcus aureus strain was grown in the presence of high concentrations of D-serine, D-threonine, and D-phenylalanine. These growth conditions resulted in the replacement of the carboxyl-terminal (fifth) D-alanine residue of peptidoglycan stem peptides with the D-amino acid present in the growth medium and a reduced ability to grow in the presence of methicillin. The most dramatic effect was seen with D-serine. With 32 mM D-serine, strains that had been able to grow in the presence of 800 micro g of methicillin per ml were only able to grow in the presence of less than 50 micro g/ml. The results also suggest that in S. aureus vancomycin resistance mediated through the incorporation of precursors not terminating in D-alanyl-D-alanine would be mutually exclusive with expression of mecA-mediated methicillin resistance. | lld:pubmed |
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pubmed-article:12234837 | pubmed:language | eng | lld:pubmed |
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pubmed-article:12234837 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12234837 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12234837 | pubmed:month | Oct | lld:pubmed |
pubmed-article:12234837 | pubmed:issn | 0066-4804 | lld:pubmed |
pubmed-article:12234837 | pubmed:author | pubmed-author:De... | lld:pubmed |
pubmed-article:12234837 | pubmed:author | pubmed-author:GageDouglasD | lld:pubmed |
pubmed-article:12234837 | pubmed:author | pubmed-author:XuNaxingN | lld:pubmed |
pubmed-article:12234837 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12234837 | pubmed:volume | 46 | lld:pubmed |
pubmed-article:12234837 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12234837 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12234837 | pubmed:pagination | 3151-5 | lld:pubmed |
pubmed-article:12234837 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:12234837 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12234837 | pubmed:articleTitle | The carboxyl terminus of peptidoglycan stem peptides is a determinant for methicillin resistance in Staphylococcus aureus. | lld:pubmed |
pubmed-article:12234837 | pubmed:affiliation | Laboratory of Microbiology, The Rockefeller University, New York, New York 10021, USA. boudewijn.dejonge@astrazeneca.com | lld:pubmed |
pubmed-article:12234837 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12234837 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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