Document Detail

Steroid receptor coactivator-1 from brain physically interacts differentially with steroid receptor subtypes.
MedLine Citation:
PMID:  18566116     Owner:  NLM     Status:  MEDLINE    
In vitro studies reveal that nuclear receptor coactivators enhance the transcriptional activity of steroid receptors, including estrogen (ER) and progestin receptors (PR), through ligand-dependent interactions. Whereas work from our laboratory and others shows that steroid receptor coactivator-1 (SRC-1) is essential for efficient ER and PR action in brain, very little is known about receptor-coactivator interactions in brain. In the present studies, pull-down assays were used to test the hypotheses that SRC-1 from hypothalamic and hippocampal tissue physically associate with recombinant PR or ER in a ligand-dependent manner. SRC-1, from hypothalamus or hippocampus, interacted with PR-A and PR-B in the presence of an agonist, but not in the absence of ligand or in the presence of a selective PR modulator, RU486. Interestingly, SRC-1 from brain associated more with PR-B, the stronger transcriptional activator, than with PR-A. In addition, SRC-1 from brain, which was confirmed by mass spectrometry, interacted with ERalpha and ERbeta in the presence of agonist but not when unliganded or in the presence of the selective ER modulator, tamoxifen. Furthermore, SRC-1 from hypothalamus, but not hippocampus, interacted more with ERalpha than ERbeta, suggesting distinct expression patterns of other cofactors in these brain regions. These findings suggest that interactions of SRC-1 from brain with PR and ER are dependent on ligand, receptor subtype, and brain region to manifest the pleiotropic functional consequences that underlie steroid-regulated behaviors. The present findings reveal distinct contrasts with previous cell culture studies and emphasize the importance of studying receptor-coactivator interactions using biologically relevant tissue.
Heather A Molenda-Figueira; Suzanne D Murphy; Katherine L Shea; Nora K Siegal; Yingxin Zhao; Joseph G Chadwick; Larry A Denner; Marc J Tetel
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2008-06-19
Journal Detail:
Title:  Endocrinology     Volume:  149     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-09-23     Completed Date:  2008-11-04     Revised Date:  2013-03-27    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5272-9     Citation Subset:  AIM; IM    
Center for Neuroendocrine Studies, Neuroscience, and Behavior Program, University of Massachusetts, Amherst, MA 01003, USA.
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MeSH Terms
Estrogen Antagonists / pharmacology
Estrogen Receptor alpha / genetics,  metabolism*
Estrogen Receptor beta / genetics,  metabolism*
Glutathione Transferase / genetics
Hippocampus / metabolism
Histone Acetyltransferases / metabolism*
Hormone Antagonists / pharmacology
Hypothalamus / metabolism*
Mass Spectrometry
Mifepristone / pharmacology
Nuclear Receptor Coactivator 1
Rats, Sprague-Dawley
Receptors, Progesterone / genetics,  metabolism*
Recombinant Proteins / genetics,  metabolism
Tamoxifen / pharmacology
Transcription Factors / metabolism*
Grant Support
Reg. No./Substance:
0/Estrogen Antagonists; 0/Estrogen Receptor alpha; 0/Estrogen Receptor beta; 0/Hormone Antagonists; 0/Ligands; 0/Receptors, Progesterone; 0/Recombinant Proteins; 0/Transcription Factors; 10540-29-1/Tamoxifen; 84371-65-3/Mifepristone; EC Acetyltransferases; EC Receptor Coactivator 1; EC Transferase

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