Linked Life Data

8261458

Source:http://linkedlifedata.com/resource/pubmed/id/8261458

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1994-1-21
pubmed:abstractText
Induction of glutathione S-transferase Ya and NAD(P)H:quinone reductase gene expression by a variety of chemical agents is mediated by regulatory elements, EpRE and ARE, composed of two adjacent AP-1-like binding sites and activated by Fos/Jun heterodimeric complex (AP-1). Recent studies show that chemical induction of glutathione S transferase Ya and quinone reductase gene expression is associated with an induction of c-fos and c-jun gene expression and AP-1 binding activity. In this report we present evidence that the AP-1 binding activity and the expression of chloramphenicol acetyltransferase activity from an EpRE Ya-cat gene construct are induced by an increase in intracellular oxidant levels. We observe that lowering the glutathione levels with buthionine sulfoximine, an inhibitor of gamma-glutamylcysteine synthetase, or diamide, a thiol-oxidizing agent, stimulates both basal and chemical-inducible expression of chloramphenicol acetyltransferase activity from EpRE Ya-cat and the AP-1 binding activity. Furthermore, we observe that the induction of these activities by a variety of chemical agents is inhibited by thiol compounds N-acetylcysteine and glutathione. These findings suggest that diverse chemicals that induce the AP-1 complex, leading to the AP-1-mediated transcriptional activation of glutathione S-transferase Ya gene expression, may act through a common mechanism involving the production of reactive oxygen species and depletion of reduced glutathione.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
54
pubmed:geneSymbol
Ya-cat, c-fos, c-jun
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
36-40
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8261458-Buthionine Sulfoximine, pubmed-meshheading:8261458-Carcinoma, Hepatocellular, pubmed-meshheading:8261458-Chloramphenicol O-Acetyltransferase, pubmed-meshheading:8261458-Diamide, pubmed-meshheading:8261458-Electron Spin Resonance Spectroscopy, pubmed-meshheading:8261458-Enzyme Induction, pubmed-meshheading:8261458-Gene Expression Regulation, Enzymologic, pubmed-meshheading:8261458-Genes, fos, pubmed-meshheading:8261458-Genes, jun, pubmed-meshheading:8261458-Glutathione, pubmed-meshheading:8261458-Glutathione Transferase, pubmed-meshheading:8261458-Humans, pubmed-meshheading:8261458-Methionine Sulfoximine, pubmed-meshheading:8261458-Proto-Oncogene Proteins c-fos, pubmed-meshheading:8261458-Proto-Oncogene Proteins c-jun, pubmed-meshheading:8261458-Tumor Cells, Cultured
pubmed:year
1994
pubmed:articleTitle
Intracellular glutathione levels regulate Fos/Jun induction and activation of glutathione S-transferase gene expression.
pubmed:affiliation
Department of Biochemistry, Weizmann Institute of Science, Rehovot, Israel.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't