pubmed-article:11553641 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11553641 | lifeskim:mentions | umls-concept:C0665341 | lld:lifeskim |
pubmed-article:11553641 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
pubmed-article:11553641 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
pubmed-article:11553641 | lifeskim:mentions | umls-concept:C1704241 | lld:lifeskim |
pubmed-article:11553641 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
pubmed-article:11553641 | pubmed:issue | 46 | lld:pubmed |
pubmed-article:11553641 | pubmed:dateCreated | 2001-11-12 | lld:pubmed |
pubmed-article:11553641 | pubmed:abstractText | The effects of estrogen and anti-estrogen are mediated through the estrogen receptors ERalpha and beta, which function as ligand-induced transcriptional factors. The nonsteroidal anti-estrogen tamoxifen is the most commonly used endocrine in the treatment of all stages of breast cancer in both pre- and postmenopausal women. Several lines of evidence have indicated that tamoxifen promotes association between ERalpha and corepressors N-CoR or silencing mediator for retinoid and thyroid hormone receptor (SMRT). Our results indicate that N-CoR/SMRT recognize and interact with helices H3 and H5 of the ERalpha ligand-binding domain in a 4-hydroxy tamoxifen-dependent manner. The mutant ERalpha(D351Y), derived from a tamoxifen-stimulated tumor and containing an amino acid substitution at position 351 within H3, showed reduced interaction with N-CoR/SMRT and high tamoxifen-induced activation function-1 (AF-1) activity. While the estradiol-dependent transcriptional activity of ERalpha(D351Y) was almost equal to that of wild-type ERalpha, the mutant exhibited higher levels of transcriptional activity in the presence of both E2 and 4-hydroxy tamoxifen compared with wild-type ERalpha. These results may explain the observation that the growth of tumor cells expressing ERalpha(D351Y) can be stimulated by tamoxifen, E2, or both. | lld:pubmed |
pubmed-article:11553641 | pubmed:language | eng | lld:pubmed |
pubmed-article:11553641 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11553641 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11553641 | pubmed:month | Nov | lld:pubmed |
pubmed-article:11553641 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:11553641 | pubmed:author | pubmed-author:WadaOO | lld:pubmed |
pubmed-article:11553641 | pubmed:author | pubmed-author:KatoSS | lld:pubmed |
pubmed-article:11553641 | pubmed:author | pubmed-author:YamamotoYY | lld:pubmed |
pubmed-article:11553641 | pubmed:author | pubmed-author:YanoTT | lld:pubmed |
pubmed-article:11553641 | pubmed:author | pubmed-author:YanagisawaJJ | lld:pubmed |
pubmed-article:11553641 | pubmed:author | pubmed-author:SuzawaMM | lld:pubmed |
pubmed-article:11553641 | pubmed:author | pubmed-author:YogiashiYY | lld:pubmed |
pubmed-article:11553641 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11553641 | pubmed:day | 16 | lld:pubmed |
pubmed-article:11553641 | pubmed:volume | 276 | lld:pubmed |
pubmed-article:11553641 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11553641 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11553641 | pubmed:pagination | 42684-91 | lld:pubmed |
pubmed-article:11553641 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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pubmed-article:11553641 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11553641 | pubmed:articleTitle | The tamoxifen-responsive estrogen receptor alpha mutant D351Y shows reduced tamoxifen-dependent interaction with corepressor complexes. | lld:pubmed |
pubmed-article:11553641 | pubmed:affiliation | Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-0034, Japan. | lld:pubmed |
pubmed-article:11553641 | pubmed:publicationType | Journal Article | lld:pubmed |
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