| pubmed-article:9280065 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C0682969 | lld:lifeskim |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C0034786 | lld:lifeskim |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C1148673 | lld:lifeskim |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C0920533 | lld:lifeskim |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:9280065 | lifeskim:mentions | umls-concept:C1709305 | lld:lifeskim |
| pubmed-article:9280065 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:9280065 | pubmed:dateCreated | 1997-10-6 | lld:pubmed |
| pubmed-article:9280065 | pubmed:abstractText | The pituitary glycoprotein hormones LH and FSH regulate the reproductive cycle and are sensitive to feedback by gonadal steroids. The common alpha-subunit shared by these hormones is transcriptionally repressed by androgen receptor (AR) in the presence of its ligand dihydrotestosterone. This identifies at least one mechanism that contributes to AR-dependent suppression of gonadotropin synthesis. Repression of alpha-subunit transcription by AR requires only the sequences within the first 480 bp of the promoter. While this region contains a high-affinity binding site for AR, this element does not mediate the suppressive effects of androgens. Instead, two other elements within the promoter-regulatory region (alpha-basal element and cAMP-regulatory element), which are important for expression of the alpha-subunit gene in gonadotropes, mediate the effects of AR. This suggests that AR inhibits activity of the alpha-subunit promoter by interfering with the transcriptional properties of the proteins that bind to alpha-basal element and the cAMP-regulatory elements. Furthermore, transfection analysis of various mutant ARs identified both the DNA-binding and ligand-binding domains of the receptor as critical for repression. Comparisons with the MMTV promoter revealed distinct structural requirements that underlie the transactivation and transrepression properties of AR. | lld:pubmed |
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| pubmed-article:9280065 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9280065 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9280065 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9280065 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9280065 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9280065 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:9280065 | pubmed:issn | 0888-8809 | lld:pubmed |
| pubmed-article:9280065 | pubmed:author | pubmed-author:WilsonE MEM | lld:pubmed |
| pubmed-article:9280065 | pubmed:author | pubmed-author:NilsonJ HJH | lld:pubmed |
| pubmed-article:9280065 | pubmed:author | pubmed-author:HeckertL LLL | lld:pubmed |
| pubmed-article:9280065 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9280065 | pubmed:volume | 11 | lld:pubmed |
| pubmed-article:9280065 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9280065 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9280065 | pubmed:pagination | 1497-506 | lld:pubmed |
| pubmed-article:9280065 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
| pubmed-article:9280065 | pubmed:meshHeading | pubmed-meshheading:9280065-... | lld:pubmed |
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| pubmed-article:9280065 | pubmed:meshHeading | pubmed-meshheading:9280065-... | lld:pubmed |
| pubmed-article:9280065 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9280065 | pubmed:articleTitle | Transcriptional repression of the alpha-subunit gene by androgen receptor occurs independently of DNA binding but requires the DNA-binding and ligand-binding domains of the receptor. | lld:pubmed |
| pubmed-article:9280065 | pubmed:affiliation | Department of Molecular and Integrative Physiology, The University of Kansas Medical Center, Kansas City 66160, USA. | lld:pubmed |
| pubmed-article:9280065 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9280065 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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