Source:http://linkedlifedata.com/resource/pubmed/id/10801832
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
28
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pubmed:dateCreated |
2000-8-16
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pubmed:abstractText |
The mechanisms that control the emergence of different anterior pituitary cells from a common stem cell population are largely unknown. The immortalized GHFT cells derived from targeted expression of SV40 T antigen to mouse pituitary display characteristics of somatolactotropic progenitors in that they express the transcription factor GHF-1 (Pit-1) but not growth hormone (GH) or prolactin (PRL). We searched for factors capable of inducing lactotropic differentiation of GHFT cells. PRL gene expression was not observed in cells subjected to a variety of stimuli, which induce PRL gene expression in mature lactotropes. Only fibroblast growth factor-2 (FGF-2) was able to initiate the transcription, synthesis, and release of PRL in GHFT cells. However, induction of PRL expression was incomplete in FGF-2-treated cells, suggesting that additional factors are necessary to attain high levels of PRL transcription in fully differentiated lactotropes. We also show that the FGF-2 response element is located in the proximal PRL promoter. Stimulation of PRL expression by FGF-2 requires endogenous Ets factors and these factors as well as GHF-1 are expressed at low levels in the committed precursor, suggesting that these low levels are limiting for full PRL expression. Moreover, FGF-2 effect on lactotrope differentiation is mediated, at least partially, by stimulation of the Ras-signaling pathway. Our results suggest that, indeed, GHFT cells represent a valid model for studying lactotropic differentiation and that FGF-2 could play a key role both in initiating lactotrope differentiation and maintaining PRL expression.
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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, Polyomavirus Transforming,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Pit1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Prolactin,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-ets,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factor Pit-1,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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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 |
14
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pubmed:volume |
275
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
21653-60
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10801832-Animals,
pubmed-meshheading:10801832-Antigens, Polyomavirus Transforming,
pubmed-meshheading:10801832-Cell Differentiation,
pubmed-meshheading:10801832-Cell Line, Transformed,
pubmed-meshheading:10801832-DNA-Binding Proteins,
pubmed-meshheading:10801832-Gene Expression Regulation,
pubmed-meshheading:10801832-Kinetics,
pubmed-meshheading:10801832-Mice,
pubmed-meshheading:10801832-Pituitary Gland, Anterior,
pubmed-meshheading:10801832-Prolactin,
pubmed-meshheading:10801832-Proto-Oncogene Proteins,
pubmed-meshheading:10801832-Proto-Oncogene Proteins c-ets,
pubmed-meshheading:10801832-RNA, Messenger,
pubmed-meshheading:10801832-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:10801832-Simian virus 40,
pubmed-meshheading:10801832-Stem Cells,
pubmed-meshheading:10801832-Transcription, Genetic,
pubmed-meshheading:10801832-Transcription Factor Pit-1,
pubmed-meshheading:10801832-Transcription Factors
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pubmed:year |
2000
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pubmed:articleTitle |
Differentiation of lactotrope precursor GHFT cells in response to fibroblast growth factor-2.
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pubmed:affiliation |
Department of Pharmacology and Center for Molecular Genetics, University of California, San Diego, La Jolla, California 92093-0636, 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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