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Interrelationship between liver X receptor alpha, sterol regulatory element-binding protein-1c, peroxisome proliferator-activated receptor gamma, and small heterodimer partner in the transcriptional regulation of glucokinase gene expression in liver

DC FieldValueLanguage
dc.contributor.author김태현-
dc.contributor.author김하일-
dc.contributor.author박주만-
dc.contributor.author배진식-
dc.contributor.author안용호-
dc.contributor.author윤호근-
dc.contributor.author김경섭-
dc.contributor.author임승순-
dc.contributor.author김미영-
dc.contributor.author차지영-
dc.date.accessioned2015-04-24T16:38:21Z-
dc.date.available2015-04-24T16:38:21Z-
dc.date.issued2009-
dc.identifier.issn0021-9258-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/103892-
dc.description.abstractLiver glucokinase (LGK) plays an essential role in controlling blood glucose levels and maintaining cellular metabolic functions. Expression of LGK is induced mainly regulated by insulin through sterol regulatory element-binding protein-1c (SREBP-1c) as a mediator. Since LGK expression is known to be decreased in the liver of liver X receptor (LXR) knockout mice, we have investigated whether LGK might be directly activated by LXRalpha. Furthermore, we have studied interrelationship between transcription factors that control gene expression of LGK. In the current studies, we demonstrated that LXRalpha increased LGK expression in primary hepatocytes and that there is a functional LXR response element in the LGK gene promoter as shown by electrophoretic mobility shift and chromatin precipitation assay. In addition, our studies demonstrate that LXRalpha and insulin activation of the LGK gene promoter occurs through a multifaceted indirect mechanism. LXRalpha increases SREBP-1c expression and then insulin stimulates the processing of the membrane-bound precursor SREBP-1c protein, and it activates LGK expression through SREBP sites in its promoter. LXRalpha also activates the LGK promoter by increasing the transcriptional activity and induction of peroxisome proliferator-activated receptor (PPAR)-gamma, which also stimulates LGK expression through a peroxisome proliferator-responsive element. This activation is tempered through a negative mechanism, where a small heterodimer partner (SHP) decreases LGK gene expression by inhibiting the transcriptional activity of LXRalpha and PPARgamma by directly interacting with their common heterodimer partner RXRalpha. From these data, we propose a mechanism for LXRalpha in controlling the gene expression of LGK that involves activation through SREBP-1c and PPARgamma and inhibition through SHP-
dc.description.statementOfResponsibilityopen-
dc.format.extent15071~15083-
dc.relation.isPartOfJOURNAL OF BIOLOGICAL CHEMISTRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHBase Sequence-
dc.subject.MESHCell Line-
dc.subject.MESHDNA-Binding Proteins/metabolism*-
dc.subject.MESHGene Expression Regulation, Enzymologic*-
dc.subject.MESHGlucokinase/genetics*-
dc.subject.MESHGlucokinase/metabolism-
dc.subject.MESHHepatocytes/enzymology-
dc.subject.MESHHumans-
dc.subject.MESHLiver/enzymology*-
dc.subject.MESHLiver X Receptors-
dc.subject.MESHMice-
dc.subject.MESHModels, Biological-
dc.subject.MESHMolecular Sequence Data-
dc.subject.MESHOrphan Nuclear Receptors-
dc.subject.MESHPPAR gamma/genetics-
dc.subject.MESHPPAR gamma/metabolism*-
dc.subject.MESHProtein Binding-
dc.subject.MESHRNA, Messenger/genetics-
dc.subject.MESHRNA, Messenger/metabolism-
dc.subject.MESHRats-
dc.subject.MESHReceptors, Cytoplasmic and Nuclear/metabolism*-
dc.subject.MESHResponse Elements/genetics-
dc.subject.MESHSterol Regulatory Element Binding Protein 1/metabolism*-
dc.subject.MESHTranscription, Genetic-
dc.titleInterrelationship between liver X receptor alpha, sterol regulatory element-binding protein-1c, peroxisome proliferator-activated receptor gamma, and small heterodimer partner in the transcriptional regulation of glucokinase gene expression in liver-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry & Molecular Biology (생화학,분자생물학)-
dc.contributor.googleauthorTae-Hyun Kim-
dc.contributor.googleauthorHail Kim-
dc.contributor.googleauthorJoo-Man Park-
dc.contributor.googleauthorSeung-Soon Im-
dc.contributor.googleauthorJin-Sik Bae-
dc.contributor.googleauthorMi-Young Kim-
dc.contributor.googleauthorHo-Geun Yoon-
dc.contributor.googleauthorJi-Young Cha-
dc.contributor.googleauthorKyung-Sup Kim-
dc.contributor.googleauthorYong-Ho Ahn-
dc.identifier.doi10.1074/jbc.M109.006742-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01092-
dc.contributor.localIdA01666-
dc.contributor.localIdA01809-
dc.contributor.localIdA02249-
dc.contributor.localIdA02625-
dc.contributor.localIdA00297-
dc.contributor.localIdA03376-
dc.contributor.localIdA00446-
dc.contributor.localIdA04008-
dc.contributor.localIdA01081-
dc.relation.journalcodeJ01258-
dc.identifier.eissn1083-351X-
dc.identifier.pmid19366697-
dc.contributor.alternativeNameKim, Tae Hyun-
dc.contributor.alternativeNameKim, Ha Il-
dc.contributor.alternativeNamePark, Joo Man-
dc.contributor.alternativeNameBae, Jin Sik-
dc.contributor.alternativeNameAhn, Yong Ho-
dc.contributor.alternativeNameYoon, Ho Geun-
dc.contributor.alternativeNameKim, Kyung Sup-
dc.contributor.alternativeNameIm, Seung Soon-
dc.contributor.alternativeNameKim, Mi Young-
dc.contributor.alternativeNameCha, Ji Young-
dc.contributor.affiliatedAuthorKim, Ha Il-
dc.contributor.affiliatedAuthorPark, Joo Man-
dc.contributor.affiliatedAuthorBae, Jin Sik-
dc.contributor.affiliatedAuthorAhn, Yong Ho-
dc.contributor.affiliatedAuthorYoon, Ho Geun-
dc.contributor.affiliatedAuthorKim, Kyung Sup-
dc.contributor.affiliatedAuthorIm, Seung Soon-
dc.contributor.affiliatedAuthorKim, Mi Young-
dc.contributor.affiliatedAuthorCha, Ji Young-
dc.contributor.affiliatedAuthorKim, Tae Hyun-
dc.citation.volume284-
dc.citation.number22-
dc.citation.startPage15071-
dc.citation.endPage15083-
dc.identifier.bibliographicCitationJOURNAL OF BIOLOGICAL CHEMISTRY, Vol.284(22) : 15071-15083, 2009-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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