Linked Life Data

8537397

Source:http://linkedlifedata.com/resource/pubmed/id/8537397

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
52
pubmed:dateCreated
1996-2-8
pubmed:abstractText
We have previously identified a silencer in the glutathione S-transferase P (GST-P) gene which is strongly and specifically expressed during chemical hepatocarcinogenesis. At least three trans-acting factors bind to multiple cis-elements in the silencer. One of them, Silencer Factor-B (SF-B), is identical with CCAAT/enhancer-binding protein beta (C/EBP beta) and binds to GST-P Silencer 1 (GPS1). Many C/EBP beta binding sites are recognized by each of the C/EBP isoforms. Western blot analyses of C/EBP isoforms during chemical hepatocarcinogenesis revealed a decrease of C/EBP alpha expression. However, there was no change in C/EBP beta level. In the nuclear extracts from normal liver, C/EBP alpha was the dominant form that bound to GPS1, whereas both C/EBP alpha and C/EBP beta bound to GPS1 in the nuclear extracts from carcinogenic liver. Furthermore, transfection assays showed that C/EBP alpha not only repressed the GST-P promoter activity but also attenuated the transcriptional stimulation by C/EBP beta. These observations strongly suggest that the ratio of C/EBP alpha to C/EBP beta is one of the important factors for the GST-P silencer activity, and the decrease of this ratio during hepatocarcinogenesis reduces the silencer activity and, consequently, increases the GST-P expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
270
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
31288-93
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
CCAAT/enhancer-binding proteins alpha and beta interact with the silencer element in the promoter of glutathione S-transferase P gene during hepatocarcinogenesis.
pubmed:affiliation
Department of Environmental Biochemistry, Faculty of Pharmaceutical Sciences, Osaka University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't