Source:http://linkedlifedata.com/resource/pubmed/id/16373364
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2006-1-26
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| pubmed:abstractText |
IL-5 is a key regulator of eosinophilic inflammation and is selectively expressed by antigen-activated Th2 lymphocytes. An important role for the proximal AP-1 and GATA sites in regulating IL-5 transcription is generally accepted but the significance of an adjacent Ets/NFAT site has remained unclear. We have investigated its role using the mouse Th2 clone D10.G4.1. Transcription of IL-5 reporter gene plasmids could be induced in D10 cells by phorbol myristate acetate/cyclic adenosine monophosphate (PMA/cAMP) stimulation and significantly further enhanced by activation of the mitogen-activated protein (MAP) kinase pathways. Strong induction of IL-5 mRNA was also induced by PMA/cAMP. Mutagenesis showed that the Ets/NFAT site is of critical importance along with the AP-1 and GATA sites in regulating IL-5 transcription stimulated by PMA/cAMP and MAP kinase activation. Transactivation was used to investigate the transcription factors which could function at the three sites and possible synergistic interactions. AP-1 (c-Fos/c-Jun) strongly induced IL-5 transcription and dominant negative AP-1 constructs confirmed that AP-1 plays an important role in regulating IL-5 expression. Ets1, unlike other members of the Ets/NFAT family, synergized strongly with AP-1 suggesting that Ets1 is the family member which functions at the Ets/NFAT site. AP-1/Ets1 transactivation also stimulated IL-5 mRNA expression. Ets1 binding to the proximal promoter region, demonstrated by chromatin immunoprecipitation, was stimulated by PMA/cAMP. The absolute dependence on the binding sites for Ets1, AP-1 and GATA-3 together with the strong synergy between Ets1 and AP-1 suggest close cooperative interactions between the three transcription factors in the regulation of IL-5 expression in mouse T cells.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/GATA3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-5,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Protein c-ets-1,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor AP-1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0953-8178
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
18
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
313-23
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:16373364-Animals,
pubmed-meshheading:16373364-Binding Sites,
pubmed-meshheading:16373364-Cyclic AMP,
pubmed-meshheading:16373364-DNA,
pubmed-meshheading:16373364-GATA3 Transcription Factor,
pubmed-meshheading:16373364-Gene Expression Regulation,
pubmed-meshheading:16373364-Genes, Reporter,
pubmed-meshheading:16373364-Genes, fos,
pubmed-meshheading:16373364-Genes, jun,
pubmed-meshheading:16373364-Interleukin-5,
pubmed-meshheading:16373364-MAP Kinase Signaling System,
pubmed-meshheading:16373364-Mice,
pubmed-meshheading:16373364-Molecular Sequence Data,
pubmed-meshheading:16373364-Mutation,
pubmed-meshheading:16373364-Promoter Regions, Genetic,
pubmed-meshheading:16373364-Protein Binding,
pubmed-meshheading:16373364-Proto-Oncogene Protein c-ets-1,
pubmed-meshheading:16373364-Tetradecanoylphorbol Acetate,
pubmed-meshheading:16373364-Th2 Cells,
pubmed-meshheading:16373364-Transcription, Genetic,
pubmed-meshheading:16373364-Transcription Factor AP-1,
pubmed-meshheading:16373364-Transcriptional Activation
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| pubmed:year |
2006
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| pubmed:articleTitle |
A role for Ets1, synergizing with AP-1 and GATA-3 in the regulation of IL-5 transcription in mouse Th2 lymphocytes.
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| pubmed:affiliation |
Division of Molecular Bioscience, John Curtin School of Medical Research, Australian National University, Mills Road, Acton, ACT 0200 Australia.
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| pubmed:publicationType |
Journal Article
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