Linked Life Data

11902729

Source:http://linkedlifedata.com/resource/pubmed/id/11902729

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-3-20
pubmed:abstractText
The vanB gene cluster mediates glycopeptide resistance by production of peptidoglycan precursors ending in the depsipeptide D-alanyl-D-lactate (D-Ala-D-Lac) instead of D-Ala-D-Ala found in susceptible enterococci. Synthesis of D-Ala-D-Lac and hydrolysis of D-Ala-D-Ala is controlled by the VanR(B)S(B) two-component regulatory system that activates transcription of the resistance genes in response to vancomycin but not to teicoplanin. Two substitutions (A3C-->G or D168-->Y) in the VanS(B) sensor kinase resulted in induction by teicoplanin, indicating that the N-terminal domain of the protein was involved in glycopeptide sensing. A substitution (T237-->K) located in the vicinity of the putative autophosphorylation site of VanS(B) (H233) was associated with a constitutive phenotype and affected a conserved residue known to be critical for the phosphatase activity of related kinases. A mutant producing an impaired host D-Ala:D-Ala ligase required vancomycin for growth, since D-Ala-D-Lac was only produced under inducing conditions. The ddl and vanS(B) mutations, alone or in combination, resulted in various resistance phenotypes that were determined by the amount of D-Ala-D-Ala and D-Ala-D-Lac incorporated into peptidoglycan precursors under different inducing conditions.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0950-382X
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
93-105
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Mutations leading to increased levels of resistance to glycopeptide antibiotics in VanB-type enterococci.
pubmed:affiliation
Unité des Agents Antibactériens, Centre National de la Recherche Scientifique EP J0058, Institut Pasteur, Paris, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't