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The Corepressors Silencing Mediator of Retinoid and Thyroid Hormone Receptor and Nuclear Receptor Corepressor Are Involved in Agonist- and Antagonist-Regulated Transcription by Androgen Receptor

DC FieldValueLanguage
dc.contributor.author윤호근-
dc.date.accessioned2015-06-10T11:52:54Z-
dc.date.available2015-06-10T11:52:54Z-
dc.date.issued2006-
dc.identifier.issn0888-8809-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/108790-
dc.description.abstractWe have investigated the role of corepressors SMRT (silencing mediator of retinoid and thyroid hormone receptor) and N-CoR (nuclear receptor corepressor) in transcriptional regulation by androgen receptor (AR) in the LNCaP prostate cancer cell line. Using specific small interference RNAs to knock down SMRT and/or N-CoR in LNCaP cells, we found that SMRT and N-CoR not only mediate antagonist-dependent inhibition of AR activation but also have a widespread role in suppressing agonist-dependent activation of several AR target genes we have tested, including PSA (prostate-specific antigen), TSC22 (TSC22 domain family member 1), NKX3–1 (NK3 transcription factor locus 1), and B2M(β-2-microglobulin). By sequencing analysis followed by analysis of physical association by chromatin immunoprecipitation assay, we mapped the putative androgen response elements in the NKX3–1 and B2M. Consistent with a role in both antagonist- and agonist-regulated transcription by AR, chromatin immunoprecipitation analysis revealed that both SMRT and N-CoR were recruited by AR to these genes in the presence of either flutamide or R1881. Knocking down SMRT and N-CoR enhanced the recruitment of the coactivators steroid receptor coactivator 1 and p300 by agonist-bound AR and led to increased hyperacetylation of histone H3 and H4, suggesting that the corepressors actively compete with coactivators for binding to agonist-bound AR. Taken together, our data indicate that SMRT and N-CoR corepressors are involved in transcriptional regulation by both agonist- and antagonist-bound AR and regulate the magnitude of hormone response, at least in part, by competing with coactivators.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1048~1060-
dc.relation.isPartOfMOLECULAR ENDOCRINOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAcetylation-
dc.subject.MESHAndrogen Receptor Antagonists-
dc.subject.MESHAndrogens-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHDNA-Binding Proteins/antagonists & inhibitors-
dc.subject.MESHDNA-Binding Proteins/genetics-
dc.subject.MESHDNA-Binding Proteins/metabolism*-
dc.subject.MESHEnhancer Elements, Genetic-
dc.subject.MESHGene Expression Regulation*-
dc.subject.MESHHistones/metabolism-
dc.subject.MESHHomeodomain Proteins/genetics-
dc.subject.MESHHumans-
dc.subject.MESHMale-
dc.subject.MESHNuclear Proteins/antagonists & inhibitors-
dc.subject.MESHNuclear Proteins/genetics-
dc.subject.MESHNuclear Proteins/metabolism*-
dc.subject.MESHNuclear Receptor Co-Repressor 1-
dc.subject.MESHNuclear Receptor Co-Repressor 2-
dc.subject.MESHProstate-Specific Antigen/genetics-
dc.subject.MESHProstatic Neoplasms/genetics-
dc.subject.MESHProstatic Neoplasms/metabolism*-
dc.subject.MESHRNA Interference-
dc.subject.MESHRNA, Small Interfering/genetics-
dc.subject.MESHRNA, Small Interfering/pharmacology-
dc.subject.MESHReceptors, Androgen/metabolism*-
dc.subject.MESHRepressor Proteins/antagonists & inhibitors-
dc.subject.MESHRepressor Proteins/genetics-
dc.subject.MESHRepressor Proteins/metabolism*-
dc.subject.MESHTranscription Factors/genetics-
dc.subject.MESHTranscription, Genetic-
dc.subject.MESHbeta 2-Microglobulin/genetics-
dc.titleThe Corepressors Silencing Mediator of Retinoid and Thyroid Hormone Receptor and Nuclear Receptor Corepressor Are Involved in Agonist- and Antagonist-Regulated Transcription by Androgen Receptor-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry & Molecular Biology (생화학,분자생물학)-
dc.contributor.googleauthorHo-Geun Yoon-
dc.contributor.googleauthorJiemin Wong-
dc.identifier.doi10.1210/me.2005-0324-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02625-
dc.relation.journalcodeJ02257-
dc.identifier.eissn1944-9917-
dc.identifier.pmid16373395-
dc.identifier.urlhttp://press.endocrine.org/doi/abs/10.1210/me.2005-0324-
dc.contributor.alternativeNameYoon, Ho Geun-
dc.contributor.affiliatedAuthorYoon, Ho Geun-
dc.rights.accessRightsnot free-
dc.citation.volume20-
dc.citation.number5-
dc.citation.startPage1048-
dc.citation.endPage1060-
dc.identifier.bibliographicCitationMOLECULAR ENDOCRINOLOGY , Vol.20(5) : 1048-1060, 2006-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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