| pubmed-article:8537397 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C1512409 | lld:lifeskim |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C1417925 | lld:lifeskim |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C1136185 | lld:lifeskim |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:8537397 | lifeskim:mentions | umls-concept:C0017833 | lld:lifeskim |
| pubmed-article:8537397 | pubmed:issue | 52 | lld:pubmed |
| pubmed-article:8537397 | pubmed:dateCreated | 1996-2-8 | lld:pubmed |
| pubmed-article:8537397 | 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. | lld:pubmed |
| pubmed-article:8537397 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8537397 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8537397 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8537397 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8537397 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8537397 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:8537397 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:8537397 | pubmed:author | pubmed-author:SuzukiTT | lld:pubmed |
| pubmed-article:8537397 | pubmed:author | pubmed-author:MuramatsuMM | lld:pubmed |
| pubmed-article:8537397 | pubmed:author | pubmed-author:ImagawaMM | lld:pubmed |
| pubmed-article:8537397 | pubmed:author | pubmed-author:NishiharaTT | lld:pubmed |
| pubmed-article:8537397 | pubmed:author | pubmed-author:TakanoKK | lld:pubmed |
| pubmed-article:8537397 | pubmed:author | pubmed-author:OsadaSS | lld:pubmed |
| pubmed-article:8537397 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8537397 | pubmed:day | 29 | lld:pubmed |
| pubmed-article:8537397 | pubmed:volume | 270 | lld:pubmed |
| pubmed-article:8537397 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8537397 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8537397 | pubmed:pagination | 31288-93 | lld:pubmed |
| pubmed-article:8537397 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:8537397 | pubmed:meshHeading | pubmed-meshheading:8537397-... | lld:pubmed |
| pubmed-article:8537397 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:8537397 | 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. | lld:pubmed |
| pubmed-article:8537397 | pubmed:affiliation | Department of Environmental Biochemistry, Faculty of Pharmaceutical Sciences, Osaka University, Japan. | lld:pubmed |
| pubmed-article:8537397 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8537397 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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