Source:http://linkedlifedata.com/resource/pubmed/id/11801594
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
14
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| pubmed:dateCreated |
2002-4-1
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| pubmed:abstractText |
Heat shock factor (HSF) 1 is the major heat shock transcription factor that regulates stress-inducible synthesis of heat shock proteins and is also essential in protection against endotoxic shock. Following our previous study, which demonstrated the transcriptional repression of the IL-1beta gene by HSF1 (Cahill, C. M., Waterman, W. R., Xie, Y., Auron, P. E., and Calderwood, S. K. (1996) J. Biol. Chem. 271, 24874-24879), we have examined the mechanisms of transcriptional repression. Our studies show that HSF1 represses the lipopolyliposaccharide-induced transcription of the IL-1beta promoter through direct interaction with the nuclear factor of interleukin 6 (NF-IL6, also known as CCAAT enhancer binding protein (C/EBPbeta), an essential regulator in IL-1beta transcription. We show for the first time that HSF1 binds directly to NF-IL6 in vivo and antagonizes its activity. The HSF1/NF-IL6 interaction involves a sequence of HSF1 containing the trimerization and regulatory domains and the bZip region of NF-IL6. HSF1 has little effect on IL-1beta promoter activity stimulated by the essential monocytic transcription factor Spi.1 but is strongly inhibitory to transcriptional activation by NF-IL6 and to the synergistic activation by NF-IL6 and Spi.1. Because of its ability to bind to specific C/EBP elements in the promoters of multiple genes and its ability to interact with other transcription factors, NF-IL6 is involved in transcriptional regulation of a wide range of genes. Interaction between HSF1 and NF-IL6 could thus be an important mechanism in HSF1 regulation of general gene transcription during endotoxin stress.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Endotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Transferase,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/heat shock transcription factor
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
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| pubmed:issn |
0021-9258
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
5
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| pubmed:volume |
277
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
11802-10
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:11801594-Animals,
pubmed-meshheading:11801594-Binding Sites,
pubmed-meshheading:11801594-Blotting, Western,
pubmed-meshheading:11801594-CHO Cells,
pubmed-meshheading:11801594-Cell Line,
pubmed-meshheading:11801594-Cell Nucleus,
pubmed-meshheading:11801594-Cricetinae,
pubmed-meshheading:11801594-DNA-Binding Proteins,
pubmed-meshheading:11801594-Endotoxins,
pubmed-meshheading:11801594-Genes, Reporter,
pubmed-meshheading:11801594-Glutathione Transferase,
pubmed-meshheading:11801594-HeLa Cells,
pubmed-meshheading:11801594-Humans,
pubmed-meshheading:11801594-Interleukin-1,
pubmed-meshheading:11801594-Interleukin-6,
pubmed-meshheading:11801594-Lipopolysaccharides,
pubmed-meshheading:11801594-Models, Biological,
pubmed-meshheading:11801594-Plasmids,
pubmed-meshheading:11801594-Precipitin Tests,
pubmed-meshheading:11801594-Promoter Regions, Genetic,
pubmed-meshheading:11801594-Protein Binding,
pubmed-meshheading:11801594-Protein Biosynthesis,
pubmed-meshheading:11801594-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:11801594-Time Factors,
pubmed-meshheading:11801594-Transcription, Genetic,
pubmed-meshheading:11801594-Transcription Factors,
pubmed-meshheading:11801594-Transcriptional Activation,
pubmed-meshheading:11801594-Transfection
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| pubmed:year |
2002
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| pubmed:articleTitle |
Heat shock factor 1 represses transcription of the IL-1beta gene through physical interaction with the nuclear factor of interleukin 6.
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| pubmed:affiliation |
Department of Radiation Oncology, Dana Farber Cancer Institute, Harvard Medical School, Beth Israel and Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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