Linked Life Data

9533460

Source:http://linkedlifedata.com/resource/pubmed/id/9533460

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-5-26
pubmed:abstractText
Using clinical strains of Serratia marcescens with low and high resistance to extended-spectrum beta-lactam antibiotics, the relative contribution of chromosomal beta-lactamase and defective outer membrane porins to resistance was determined. Low-level resistance was caused by overproduced beta-lactamase alone. High-level resistance was due to beta-lactamase overproduction and defects of porin OmpF or OmpF and OmpC. Overproduction of beta-lactamase in bacteria with both degrees of resistance was eliminated by transformation with cloned ampD+, the gene (from Escherichia coli) for negative modulation of beta-lactamase induction. In transformants of highly resistant bacteria with normally low and inducible beta-lactamase production, the remaining porin defects alone imparted only minimal resistance to extended-spectrum beta-lactam antibiotics.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0305-7453
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
189-95
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Contribution of overproduced chromosomal beta-lactamase and defective outer membrane porins to resistance to extended-spectrum beta-lactam antibiotics in Serratia marcescens.
pubmed:affiliation
Institut für Mikrobiologie, Technische Hochschule Darmstadt, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't