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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
1996-7-9
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pubmed:abstractText |
The orphan nuclear receptor, steroidogenic factor-1 (SF-1), is expressed in the pituitary and in the gonadotrope precursor cell line, alphaT3-1, where it is believed to enhance expression of the common gonadotropin alpha-subunit gene through transactivation of the gonadotrope-specific element (GSE). Sequence analysis of the rat luteinizing hormone beta-subunit (LH beta) gene promoter revealed the presence of a consensus GSE at -127 to -119 (TGACCTTGT). We have demonstrated the ability of SF-1 to bind specifically to this putative GSE sequence by electrophoretic mobility shift assay, utilizing both alphaT3-1 nuclear extracts and in vitro translated SF-1. In addition, mutation of the putative LHbeta-GSE (TGAAATTGT) eliminated specific DNA binding. To examine the ability of SF-1 to enhance LHbeta promoter activity, CV-1 cells, which lack endogenous SF-1, were cotransfected with an SF-1-containing expression vector and an LHbeta-luciferase reporter construct. When cotransfected with -209/+5 of the LHbeta promoter, SF-1 increased luciferase activity by 56-fold. SF-1 responsiveness was markedly diminished with loss of the putative GSE region in deletion constructs and in the presence of a two base pair mutation, analogous to the mutation which eliminated DNA binding. Finally, the LHbeta-GSE was able to confer SF-1 responsiveness on a heterologous minimal growth hormone promoter, GH50 (57-fold). We conclude that SF-1 both binds to and transactivates the rat LHbeta promoter. These data suggest that SF-1 may participate in the expression of the LHbeta gene by the gonadotrope.
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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,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Fushi Tarazu Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Luteinizing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Steroidogenic Factor 1,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/steroidogenic factor 1, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/steroidogenic factor 1, rat
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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 |
6645-50
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8636081-Animals,
pubmed-meshheading:8636081-Base Sequence,
pubmed-meshheading:8636081-Cell Line,
pubmed-meshheading:8636081-DNA,
pubmed-meshheading:8636081-DNA-Binding Proteins,
pubmed-meshheading:8636081-Fushi Tarazu Transcription Factors,
pubmed-meshheading:8636081-Haplorhini,
pubmed-meshheading:8636081-Homeodomain Proteins,
pubmed-meshheading:8636081-Luteinizing Hormone,
pubmed-meshheading:8636081-Mice,
pubmed-meshheading:8636081-Molecular Sequence Data,
pubmed-meshheading:8636081-Mutation,
pubmed-meshheading:8636081-Promoter Regions, Genetic,
pubmed-meshheading:8636081-Protein Biosynthesis,
pubmed-meshheading:8636081-Rats,
pubmed-meshheading:8636081-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:8636081-Steroidogenic Factor 1,
pubmed-meshheading:8636081-Transcription Factors
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pubmed:year |
1996
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pubmed:articleTitle |
Stimulation of luteinizing hormone beta gene promoter activity by the orphan nuclear receptor, steroidogenic factor-1.
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pubmed:affiliation |
Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, 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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