Source:http://linkedlifedata.com/resource/pubmed/id/15123623
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
30
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| pubmed:dateCreated |
2004-7-19
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| pubmed:abstractText |
The GATA family of transcription factors establishes genetic networks that control developmental processes including hematopoiesis, vasculogenesis, and cardiogenesis. We found that GATA-1 strongly activates transcription of the Tac-2 gene, which encodes proneurokinin-B, a precursor of neurokinin-B (NK-B). Neurokinins function through G protein-coupled transmembrane receptors to mediate diverse physiological responses including pain perception and the control of vascular tone. Whereas an elevated level of NK-B was implicated in pregnancy-associated pre-eclampsia (Page, N. M., Woods, R. J., Gardiner, S. M., Lomthaisong, K., Gladwell, R. T., Butlin, D. J., Manyonda, I. T., and Lowry, P. J. (2000) Nature 405, 797-800), the regulation of NK-B synthesis and function are poorly understood. Tac-2 was expressed in normal murine erythroid cells and was induced upon ex vivo erythropoiesis. An estrogen receptor fusion to GATA-1 (ER-GATA-1) and endogenous GATA-1 both occupied a region of Tac-2 intron-7, which contains two conserved GATA motifs. Genetic complementation analysis in GATA-1-null G1E cells revealed that endogenous GATA-2 occupied the same region of intron-7, and expression of ER-GATA-1 displaced GATA-2 and activated Tac-2 transcription. Erythroid cells did not express neurokinin receptors, whereas aortic and yolk sac endothelial cells differentially expressed neurokinin receptor subtypes. Since NK-B induced cAMP accumulation in yolk sac endothelial cells, these results suggest a new mode of vascular regulation in which GATA-1 controls NK-B synthesis in erythroid cells.
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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 Primers,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Erythroid-Specific DNA-Binding...,
http://linkedlifedata.com/resource/pubmed/chemical/GATA1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/GATA1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Gata1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Neurokinin B,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tachykinins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/preprotachykinin
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0021-9258
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
23
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| pubmed:volume |
279
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
31348-56
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:15123623-Animals,
pubmed-meshheading:15123623-Base Sequence,
pubmed-meshheading:15123623-Cell Line,
pubmed-meshheading:15123623-DNA Primers,
pubmed-meshheading:15123623-DNA-Binding Proteins,
pubmed-meshheading:15123623-Erythroid Cells,
pubmed-meshheading:15123623-Erythroid-Specific DNA-Binding Factors,
pubmed-meshheading:15123623-Female,
pubmed-meshheading:15123623-GATA1 Transcription Factor,
pubmed-meshheading:15123623-Humans,
pubmed-meshheading:15123623-Mice,
pubmed-meshheading:15123623-Mice, Inbred C57BL,
pubmed-meshheading:15123623-Models, Biological,
pubmed-meshheading:15123623-Neurokinin B,
pubmed-meshheading:15123623-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:15123623-Protein Precursors,
pubmed-meshheading:15123623-RNA, Messenger,
pubmed-meshheading:15123623-Tachykinins,
pubmed-meshheading:15123623-Transcription Factors,
pubmed-meshheading:15123623-Transcriptional Activation
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| pubmed:year |
2004
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| pubmed:articleTitle |
Neurokinin-B transcription in erythroid cells: direct activation by the hematopoietic transcription factor GATA-1.
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| pubmed:affiliation |
University of Wisconsin Medical School, Molecular and Cellular Pharmacology Program, Department of Pharmacology, Madison, Wisconsin 53706, USA.
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| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
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