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Sequential phosphorylation of CCAAT enhancer-binding protein beta by MAPK and glycogen synthase kinase 3 beta is required for adipogenesis

DC FieldValueLanguage
dc.contributor.author김재우-
dc.date.accessioned2015-08-26T16:43:21Z-
dc.date.available2015-08-26T16:43:21Z-
dc.date.issued2005-
dc.identifier.issn0027-8424-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/114970-
dc.description.abstractCCAAT enhancer-binding protein (C/EBP)β, C/EBPα, and peroxisome proliferator activated receptor (PPAR)γ act in a cascade where C/EBPβ activates expression of C/EBPα and PPARγ, which then function as pleiotropic activators of genes that produce the adipocyte phenotype. When growth-arrested 3T3-L1 preadipocytes are induced to differentiate, C/EBPβ is rapidly expressed but still lacks DNA-binding activity. After a long (14-hour) lag, glycogen synthase kinase 3β enters the nucleus, which correlates with hyperphosphorylation of C/EBPβ and acquisition of DNA-binding activity. Concurrently, 3T3-L1 preadipocytes synchronously enter S phase and undergo mitotic clonal expansion, a prerequisite for terminal differentiation. Ex vivo and in vitro experiments with C/EBPβ show that phosphorylation of Thr-188 by mitogen-activating protein kinase “primes” C/EBPβ for subsequent phosphorylation on Ser-184 and Thr-179 by glycogen synthase kinase 3β, acquisition of DNA-binding function, and transactivation of the C/EBPα and PPARγ genes. The delayed transactivation of the C/EBPα and PPARγ genes by C/EBPβ appears necessary to allow mitotic clonal expansion, which would otherwise be prevented, because C/EBPα and PPARγ are antimitotic.-
dc.description.statementOfResponsibilityopen-
dc.format.extent9766~9771-
dc.relation.isPartOfPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESH3T3-L1 Cells-
dc.subject.MESHAdipocytes/cytology*-
dc.subject.MESHAdipocytes/metabolism-
dc.subject.MESHAnimals-
dc.subject.MESHCCAAT-Enhancer-Binding Protein-beta/metabolism*-
dc.subject.MESHCell Differentiation/physiology*-
dc.subject.MESHCell Nucleus/metabolism-
dc.subject.MESHChromatin Immunoprecipitation-
dc.subject.MESHChromatography, Liquid-
dc.subject.MESHElectrophoresis, Polyacrylamide Gel-
dc.subject.MESHGlycogen Synthase Kinase 3/metabolism*-
dc.subject.MESHGlycogen Synthase Kinase 3 beta-
dc.subject.MESHImmunoblotting-
dc.subject.MESHIsoelectric Focusing-
dc.subject.MESHMass Spectrometry-
dc.subject.MESHMice-
dc.subject.MESHMitogen-Activated Protein Kinases/metabolism*-
dc.subject.MESHPPAR gamma/metabolism-
dc.subject.MESHPhosphorylation-
dc.subject.MESHTranscriptional Activation/physiology-
dc.titleSequential phosphorylation of CCAAT enhancer-binding protein beta by MAPK and glycogen synthase kinase 3 beta is required for adipogenesis-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Biochemistry & Molecular Biology (생화학,분자생물학)-
dc.contributor.googleauthorQi-Qun Tang-
dc.contributor.googleauthorMads Grønborg-
dc.contributor.googleauthorM. Daniel Lane-
dc.contributor.googleauthorAkhilesh Pandey-
dc.contributor.googleauthorTamara C. Otto-
dc.contributor.googleauthorJae-Woo Kim-
dc.contributor.googleauthorHaiyan Huang-
dc.identifier.doi10.1073/pnas.0503891102-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00865-
dc.relation.journalcodeJ02550-
dc.identifier.eissn1091-6490-
dc.identifier.pmid15985551-
dc.subject.keyword3T3-L1 preadipocyte-
dc.subject.keywordcell cycle-
dc.subject.keyworddifferentiation-
dc.subject.keywordmitotic clonal expansion-
dc.contributor.alternativeNameKim, Jae Woo-
dc.contributor.affiliatedAuthorKim, Jae Woo-
dc.rights.accessRightsfree-
dc.citation.volume102-
dc.citation.number28-
dc.citation.startPage9766-
dc.citation.endPage9771-
dc.identifier.bibliographicCitationPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol.102(28) : 9766-9771, 2005-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers

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