Abstract:
:The mechanisms by which SF-1 (Steroidogenic Factor-1) and Dax-1 (Dosage-sensitive sex reversal-Adrenal hypoplasia congenita critical region on the X chromosome) dictate adrenal-specific transcriptional programs are the focus of this laboratory. SF-1-mediated transcription is upregulated by phosphorylation of serine 203 located in the hinge region of SF-1. An SF-1S203A mutant attenuates SF-1 activation, while substitution of S203 with a charged aspartate (SF-1S203D) results in a dose dependent increase in SF-1 mediated transcription. Ser203 serves as a substrate for Erk2 in vitro and is critical for activation of SF-1 by multiple components of the MAPK pathway. Isoelectric focusing demonstrates multiple immuno-reactive SF-1 species in mouse adrenal and NCI-H295A cell extracts. We propose that differential phosphorylation of SF-1 by various mitogens serves to couple extracellular signals to adrenal-specific transcriptional programs. Mouse studies utilizing SF-1 heterozygous mice explore the in vivo role of SF-1 levels, SF-1 phosphorylation and SF-1 interaction with Dax-1 in adrenal steroidogenesis. SF-1 heterozygous mice exhibit a marked decrease in baseline and post-stress corticosterone with a concomitant increase in ACTH. The role of Dax-1 in these SF-1 dependent processes is explored in compound SF-1 (+/-)/Dax-1 KO mice that exhibit an increase in basal corticosterone and a decrease in basal ACTH compared to simple SF-1 (+/-) mice. These finding are consistent with an inhibitory role for Dax-1 in SF-1 mediated transcription. Mice that express epitope tagged SF-1 (wild type, SF-1S203A and SF-1S203D) are being used to rescue the heterozygous adrenal phenotype and to determine the in vivo role of SF-1 phosphorylation in adrenal function.
journal_name
Endocr Resjournal_title
Endocrine researchauthors
Babu PS,Bavers DL,Shah S,Hammer GDdoi
10.3109/07435800009048628subject
Has Abstractpub_date
2000-11-01 00:00:00pages
985-94issue
4eissn
0743-5800issn
1532-4206journal_volume
26pub_type
杂志文章abstract:INTRODUCTION:Impairments in neuroendocrine regulation of food intake and postprandial satiety are leading causes to obesity. Ghrelin peptide is a GI hormone known to increase food intake partly through induction of growth hormone. The regulation of ghrelin production is still unknown. OBJECTIVE:The aim of the current ...
journal_title:Endocrine research
pub_type: 杂志文章
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更新日期:2014-01-01 00:00:00
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journal_title:Endocrine research
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journal_title:Endocrine research
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journal_title:Endocrine research
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journal_title:Endocrine research
pub_type: 杂志文章
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journal_title:Endocrine research
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更新日期:2012-01-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
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更新日期:2004-02-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
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journal_title:Endocrine research
pub_type: 杂志文章
doi:10.3109/07435800.2012.733987
更新日期:2013-08-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
doi:10.3109/07435809809032628
更新日期:1998-08-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
doi:10.1080/07435800500371748
更新日期:2005-01-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章,评审
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更新日期:1989-01-01 00:00:00
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更新日期:2015-01-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
doi:10.1080/07435809009033011
更新日期:1990-01-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
doi:10.1081/erc-120015059
更新日期:2002-08-01 00:00:00
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journal_title:Endocrine research
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更新日期:2004-05-01 00:00:00
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journal_title:Endocrine research
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更新日期:1988-01-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
doi:10.1080/07435809609043775
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doi:10.3109/07435800.2016.1173056
更新日期:2017-02-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
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更新日期:1994-05-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章
doi:10.1081/erc-200043623
更新日期:2004-11-01 00:00:00
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journal_title:Endocrine research
pub_type: 杂志文章,评审
doi:10.1080/07435809609043755
更新日期:1996-11-01 00:00:00
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更新日期:2002-11-01 00:00:00
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journal_title:Endocrine research
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更新日期:2000-05-01 00:00:00
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更新日期:2002-02-01 00:00:00
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journal_title:Endocrine research
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更新日期:2002-11-01 00:00:00
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更新日期:2018-11-01 00:00:00