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Role of 14-3-3η as a Positive Regulator of the Glucocorticoid Receptor Transcriptional Activation

DC Field Value Language
dc.contributor.author고형준-
dc.contributor.author권오웅-
dc.contributor.author이성철-
dc.contributor.author이준행-
dc.date.accessioned2017-05-04T07:37:49Z-
dc.date.available2017-05-04T07:37:49Z-
dc.date.issued2005-
dc.identifier.issn0013-7227-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/147560-
dc.description.abstractThe glucocorticoid receptor (GR), a member of the nuclear receptor superfamily, mediates the effects of glucocorticoids. It is known that 14-3-3 family proteins interact with GR and regulate its transcriptional activity. They also bind to several molecules and influence many cellular events by altering their subcellular localization and/or acting as a chaperone. Recently, it has been proposed that ligand-activated degradation of GR occurs via the ubiquitin-proteasomal degradation pathway and that inhibition of proteasomal activity induces up-regulation of GR and enhances the transcriptional activity of GR. To examine the function of 14-3-3eta in the glucocorticoid-dependent signal pathway, we studied the regulatory role of 14-3-3eta in ligand-induced GR transcriptional activation. 14-3-3eta Enhanced the transcriptional activity of GR, and the levels of GR were higher in cells transfected with the 14-3-3eta expression vector in response to glucocorticoid. The GR level increased in both cytosol and nucleus, and endogenous GR was also elevated by 14-3-3eta in HeLa cells. 14-3-3eta Inhibited ligand-induced down-regulation of GR. Proteasomal inhibition did not induce any synergistic effect on the 14-3-3eta-induced increase in GR in response to glucocorticoid, and inhibition of translation did not block elevation of GR by 14-3-3eta, indicating that 14-3-3eta induces stabilization of GR. These results suggest that 14-3-3eta functions as a positive regulator in the glucocorticoid signal pathway by blocking the degradation of GR and inducing an elevation of GR, thus enhancing the transcriptional activity of GR.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherEndocrine Society-
dc.relation.isPartOfENDOCRINOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESH14-3-3 Proteins/physiology*-
dc.subject.MESHAnimals-
dc.subject.MESHCOS Cells-
dc.subject.MESHCercopithecus aethiops-
dc.subject.MESHDexamethasone/pharmacology-
dc.subject.MESHDown-Regulation/drug effects-
dc.subject.MESHDown-Regulation/physiology-
dc.subject.MESHDrug Stability-
dc.subject.MESHGlucocorticoids/pharmacology-
dc.subject.MESHHeLa Cells-
dc.subject.MESHHumans-
dc.subject.MESHReceptors, Glucocorticoid/chemistry-
dc.subject.MESHReceptors, Glucocorticoid/genetics*-
dc.subject.MESHReceptors, Glucocorticoid/metabolism-
dc.subject.MESHTranscriptional Activation/drug effects-
dc.subject.MESHTranscriptional Activation/physiology*-
dc.titleRole of 14-3-3η as a Positive Regulator of the Glucocorticoid Receptor Transcriptional Activation-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Ophthalmology (안과학교실)-
dc.contributor.departmentDept. of Ophthalmology (안과학교실)-
dc.contributor.departmentDept. of Ophthalmology (안과학교실)-
dc.contributor.departmentDept. of Ophthalmology (안과학교실)-
dc.contributor.googleauthorYoon Suk Kim-
dc.contributor.googleauthorSung-Wuk Jang-
dc.contributor.googleauthorHo Joong Sung-
dc.contributor.googleauthorHye Jin Lee-
dc.contributor.googleauthorIn Sik Kim-
dc.contributor.googleauthorDoe Sun Na-
dc.contributor.googleauthorJesang Ko-
dc.identifier.doi10.1210/en.2004-1455-
dc.contributor.localIdA00152-
dc.contributor.localIdA00235-
dc.contributor.localIdA02873-
dc.contributor.localIdA03180-
dc.relation.journalcodeJ00772-
dc.identifier.eissn1945-7170-
dc.identifier.pmid15790729-
dc.identifier.urlhttp://press.endocrine.org/doi/abs/10.1210/en.2004-1455-
dc.subject.keyword15790729-
dc.contributor.alternativeNameKoh, Hyoung Jun-
dc.contributor.alternativeNameKwon, Oh Woong-
dc.contributor.alternativeNameLee, Sung Chul-
dc.contributor.alternativeNameLee, Joon Haeng-
dc.citation.volume146-
dc.citation.number7-
dc.citation.startPage3133-
dc.citation.endPage3140-
dc.identifier.bibliographicCitationENDOCRINOLOGY, Vol.146(7) : 3133-3140, 2005-
dc.date.modified2017-05-04-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers

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