| pubmed-article:7531820 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0034804 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0001443 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0014930 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0752229 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0332257 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0439596 | lld:lifeskim |
| pubmed-article:7531820 | lifeskim:mentions | umls-concept:C0205254 | lld:lifeskim |
| pubmed-article:7531820 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:7531820 | pubmed:dateCreated | 1995-3-13 | lld:pubmed |
| pubmed-article:7531820 | pubmed:abstractText | We show that some transcriptionally inactive human estrogen receptor (ER) mutants can be activated by 17 beta-estradiol (E2), and sometimes by antiestrogens, in the presence of elevated levels of intracellular cAMP. ER-deficient Chinese hamster ovary or 3T3 mouse fibroblast cells were transfected with mutant ERs (the point mutant L540Q, the frameshift mutant S554fs, or the carboxy-terminal truncated receptor ER1-530) and various estrogen response element-containing reporter genes. Individual treatments with E2, the antiestrogens trans-hydroxytamoxifen and ICI 164,384, or with 3-isobutyl-1-methyl-xanthine plus cholera toxin (IBMX plus CT) which raise intracellular cAMP, generally do not activate the mutant receptors. However, cotreatment with IBMX/CT and one of the three ligands (E2, trans-hydroxytamoxifen, or ICI164,384) results in the unexpected recovery of strong activation of the L540Q or S554fs receptors, the magnitude of which is dependent upon promoter- and cell-contexts. Unlike L540Q and S554fs, the transcriptionally inactive ER1-530 is not activated by any combination of ligands and IBMX/CT. These data demonstrate that some ER mutants that form transcriptionally nonproductive ER-E2 complexes can be successfully activated by the combination of an agonist or antagonist ligand and an agent thought to act via phosphorylation pathways. Also highlighted is the promoter- and cell-specific nature of the transcriptional response to different ligand-ER complexes. Lastly, the enhanced transcriptional activity of wild type ER and some ER mutants in the presence of antiestrogens and elevated intracellular cAMP may provide a partial explanation of the ability of some estrogen-dependent human breast tumors to resist antiestrogen therapies currently employed. | lld:pubmed |
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| pubmed-article:7531820 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7531820 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7531820 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7531820 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7531820 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:7531820 | pubmed:issn | 0888-8809 | lld:pubmed |
| pubmed-article:7531820 | pubmed:author | pubmed-author:Katzenellenbo... | lld:pubmed |
| pubmed-article:7531820 | pubmed:author | pubmed-author:MontanoM MMM | lld:pubmed |
| pubmed-article:7531820 | pubmed:author | pubmed-author:InceB ABA | lld:pubmed |
| pubmed-article:7531820 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7531820 | pubmed:volume | 8 | lld:pubmed |
| pubmed-article:7531820 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7531820 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7531820 | pubmed:pagination | 1397-406 | lld:pubmed |
| pubmed-article:7531820 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:7531820 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7531820 | pubmed:articleTitle | Activation of transcriptionally inactive human estrogen receptors by cyclic adenosine 3',5'-monophosphate and ligands including antiestrogens. | lld:pubmed |
| pubmed-article:7531820 | pubmed:affiliation | Department of Physiology and Biophysics, University of Illinois, Urbana 61801. | lld:pubmed |
| pubmed-article:7531820 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7531820 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7531820 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:7531820 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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