rdf:type |
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lifeskim:mentions |
umls-concept:C0017337,
umls-concept:C0033684,
umls-concept:C0036734,
umls-concept:C0040649,
umls-concept:C0040661,
umls-concept:C0227525,
umls-concept:C0443299,
umls-concept:C0851285,
umls-concept:C1705162,
umls-concept:C1710082,
umls-concept:C2717971
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pubmed:issue |
12
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pubmed:dateCreated |
1996-7-9
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pubmed:abstractText |
The serine proteinase inhibitor (SPI-3) gene expression is transcriptionally regulated by interleukin (IL)-6 and glucocorticoids in hepatic cells. To identify the transcription factors involved in regulation of the SPI-3 promoter-chloramphenicol acetyltransferase constructs we overexpressed Signal Transducer and Activator of Transcription (STAT) proteins (STAT1, STAT3, STAT5B, and STAT6) and CAAT enhancer-binding protein beta. Specific signaling pathways were activated by cointroduced receptors for growth hormone, IL-3, IL-4, or chimeric receptors containing the cytoplasmic domain of gp130. STAT3 and STAT5B induced transcription via the SPI-3 promoter. The STAT5B response was substantially enhanced by truncation of the 5'-flanking region from -1021 to -148. The responsiveness to STAT3 and STAT5B required the STAT binding element at -132 to -124. This element was sufficient to confer regulation onto a heterologous promoter gene construct. In contrast, overexpression of CAAT enhancer-binding protein beta reduced the transcriptional activity of the SPI-3 promoter, presumably by interfering with STAT protein binding to the promoter element. The SPI-3 gene is the first example of an acute phase gene that is responsive to both STAT3 and STAT5B.
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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/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokine Receptor gp130,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Il6st protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Milk Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT5 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Serine Proteinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Stat3 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Stat5b protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0021-9258
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:day |
22
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pubmed:volume |
271
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6752-7
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8636096-Animals,
pubmed-meshheading:8636096-Antigens, CD,
pubmed-meshheading:8636096-Base Sequence,
pubmed-meshheading:8636096-Cell Line,
pubmed-meshheading:8636096-Cytokine Receptor gp130,
pubmed-meshheading:8636096-DNA Primers,
pubmed-meshheading:8636096-DNA-Binding Proteins,
pubmed-meshheading:8636096-Liver,
pubmed-meshheading:8636096-Membrane Glycoproteins,
pubmed-meshheading:8636096-Milk Proteins,
pubmed-meshheading:8636096-Molecular Sequence Data,
pubmed-meshheading:8636096-Rats,
pubmed-meshheading:8636096-STAT3 Transcription Factor,
pubmed-meshheading:8636096-STAT5 Transcription Factor,
pubmed-meshheading:8636096-Serine Proteinase Inhibitors,
pubmed-meshheading:8636096-Trans-Activators,
pubmed-meshheading:8636096-Transcription, Genetic
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pubmed:year |
1996
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pubmed:articleTitle |
Two separate signal transducer and activator of transcription proteins regulate transcription of the serine proteinase inhibitor-3 gene in hepatic cells.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, The University of Georgia, Athens, Georgia 306022, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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