Linked Life Data

10362527

Source:http://linkedlifedata.com/resource/pubmed/id/10362527

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-6-28
pubmed:abstractText
The cop operon of Enterococcus hirae encodes a repressor, CopY, a copper chaperone, CopZ, and two copper ATPases, CopA and CopB. Regulation of the cop operon is bi-phasic, with copper addition as well as copper chelation leading to induction. Using a plasmid-borne system with a reporter gene, induction of wild-type and mutant cop promoters by high and low copper conditions was investigated. Only mutations that impaired the interaction of CopY with both DNA binding sites had a marked effect on regulation, leading to hyperinduction by copper(I) or copper(II). Chelation of copper(II), but not copper(I), also induced the operon, but induction by copper chelation was not significantly affected by the mutations. E. hirae mutants with reduced extracellular copper reductase activity exhibited the same induction kinetics as wild-type cells. These results show that copper addition and copper chelation induce the cop operon by different routes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-291X
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:day
7
pubmed:volume
259
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
443-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1999
pubmed:articleTitle
Effects of promoter mutations on the in vivo regulation of the cop operon of Enterococcus hirae by copper(I) and copper(II).
pubmed:affiliation
Department of Clinical Pharmacology, University of Berne, Berne, 3010, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't