Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
|
| pubmed:dateCreated |
1997-11-12
|
| pubmed:abstractText |
The human T-cell leukemia virus type I (HTLV-I), which infects a wide variety of mammalian cells including monocytes and macrophages, encodes a transactivating protein designated as Tax. We now report that Tax induces the human prointerleukin-1beta (IL1B) gene promoter in monocytic cells. In our transient transfection assays using human THP-1 monocytic cells, a chloramphenicol acetyltransferase (CAT) construct containing the IL1B promoter sequence between positions -131 and +12 showed an approximately 90-fold increase in activity following cotransfection of a Tax expression vector. Moreover, Tax synergized with lipopolysaccharide (LPS) to induce the IL1B promoter activity. Analyses of specific nucleotide substitutions further indicated that the Tax-induced transcriptional activation requires two transcription factor binding motifs within the IL1B promoter; one is a binding site for nuclear factor (NF)-IL6 (CCAAT/enhancer binding protein beta, C/EBP beta), which belongs to the basic region-leucine zipper (bZIP) family and the other for Spi-1 (PU.1), which is an Ets family protein found principally in monocytes, macrophages, and B lymphocytes. In electrophoretic mobility shift assays (EMSA) using in vivo THP-1 nuclear extracts, Tax expression in THP-1 monocytic cells significantly increased binding of the two factors to their target IL1B promoter sequences. However, in contrast to NF-IL6 and Spi-1, DNA binding activity of Oct-1, an ubiquitously expressed octamer-binding protein was not affected by Tax. Additional EMSA using in vitro translated proteins also showed that recombinant Tax enhances DNA binding of both of recombinant NF-IL6 and Spi-1 proteins. These data were supported by our glutathione S-transferase (GST)-pull-down data, which indicated that Tax physically interacts with the two proteins. Based on the results obtained from the present study, we conclude that the IL1B promoter is a Tax-responsive sequence as a result of ability of Tax to induce binding of NF-IL6 and Spi-1 to the IL1B promoter sequence through protein-protein interaction.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCAAT-Enhancer-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, tax,
http://linkedlifedata.com/resource/pubmed/chemical/HCFC1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Host Cell Factor C1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Octamer Transcription Factor-1,
http://linkedlifedata.com/resource/pubmed/chemical/POU2F1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/interleukin 1 precursor,
http://linkedlifedata.com/resource/pubmed/chemical/proto-oncogene protein Spi-1
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0006-4971
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
90
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3142-53
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:9376596-Binding Sites,
pubmed-meshheading:9376596-CCAAT-Enhancer-Binding Proteins,
pubmed-meshheading:9376596-Cells, Cultured,
pubmed-meshheading:9376596-DNA,
pubmed-meshheading:9376596-DNA-Binding Proteins,
pubmed-meshheading:9376596-Gene Products, tax,
pubmed-meshheading:9376596-Host Cell Factor C1,
pubmed-meshheading:9376596-Human T-lymphotropic virus 1,
pubmed-meshheading:9376596-Humans,
pubmed-meshheading:9376596-Interleukin-1,
pubmed-meshheading:9376596-Nuclear Proteins,
pubmed-meshheading:9376596-Octamer Transcription Factor-1,
pubmed-meshheading:9376596-Promoter Regions, Genetic,
pubmed-meshheading:9376596-Protein Binding,
pubmed-meshheading:9376596-Protein Precursors,
pubmed-meshheading:9376596-Proto-Oncogene Proteins,
pubmed-meshheading:9376596-Trans-Activators,
pubmed-meshheading:9376596-Transcription Factors,
pubmed-meshheading:9376596-Transcriptional Activation
|
| pubmed:year |
1997
|
| pubmed:articleTitle |
Human T-cell leukemia virus type I Tax transactivates the promoter of human prointerleukin-1beta gene through association with two transcription factors, nuclear factor-interleukin-6 and Spi-1.
|
| pubmed:affiliation |
First Department of Internal Medicine, School of Medicine and the School of Health Sciences, University of Occupational and Environmental Health, Kitakyushu, Japan.
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| pubmed:publicationType |
Journal Article
|