Linked Life Data

8609888

Source:http://linkedlifedata.com/resource/pubmed/id/8609888

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-5-30
pubmed:abstractText
We examined the effects of various metal ions on the DNA-binding activity of the glucocorticoid receptor. Electrophoretic mobility shift assays demonstrated that the sequence-specific DNA binding activity of the receptor was decreased by metal ions in a dose-dependent fashion. The most potent inhibitor was Au(I). Cu(II), Cd(II), and Zn(II) were, in that order, less potent as inhibitors, whereas Fe(III), Al(III), and Mg(II) had no apparent effect. The inhibitory actions of metal ions were efficiently counteracted by the sulfhydryl reducing reagents 2-mercaptoethanol and N-acetyl-L-cysteine, indicating that metal ions interfere with the DNA binding activity of the glucocorticoid receptor through modification of sulfhydryl groups in the receptor molecule. Modification of sulfhydryls by metals seems to involve neither disulfide bond formation nor permanent destruction of the GR protein and is reversible. We also show that metal ions inhibit glucocorticoid-inducible gene transcription in vivo, presumably by interfering with the interaction between the glucocorticoid receptor and cognate DNA target sequences. In summary, these data demonstrates that metal ions are capable of modulating glucocorticoid receptor mediated intracellular signalling pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0026-895X
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
612-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Modulation of glucocorticoid-inducible gene expression by metal ions.
pubmed:affiliation
Second Department of Internal Medicine, Asahikawa Medical College, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't