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Article: Role of CREB in Transcriptional Regulation of CCAAT/Enhancer-binding Protein β Gene during Adipogenesis

TitleRole of CREB in Transcriptional Regulation of CCAAT/Enhancer-binding Protein β Gene during Adipogenesis
Authors
Issue Date2004
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2004, v. 279 n. 6, p. 4471-4478 How to Cite?
AbstractThe proximal promoter of the C/EBPβ gene possesses dual cis regulatory elements (TGA1 and TGA2), both of which contain core CREB binding sites. Comparison of the activities of C/EBPβ promoter-reporter genes with 5′-truncations or site-directed mutations in the TGA elements showed that both are required for maximal promoter function. Electrophoretic mobility shift and chromatin immunoprecipitation (ChIP) analyses with antibodies specific to CREB and ATF1 showed that these CREB family members associate with the proximal promoter both in vitro and ex vivo. Immunoblotting and ChIP analysis revealed that other CREB family members, CREM and ATF1, are up-regulated and associate with the proximal C/EBPβ promoter in mouse embryonic fibroblasts (MEFs) from CREB(-/-) mice. ChIP analysis of wild-type MEFs and 3T3-L1 preadipocytes revealed that interaction of phospho-CREB, the active form of CREB, with the C/EBPβ gene promoter occurs only after induction of differentiation of 3T3-L1 preadipocytes and MEFs. Consistent with the interaction of CREB and ATF1 at the TGA regulatory elements, expression of constitutively active CREB strongly activated C/EBPβ promoter-reporter genes, induced expression of endogenous C/EBPβ, and caused adipogenesis in the absence of the hormonal inducers normally required. Conversely, expression of a dominant-negative CREB blocked promoter-reporter activity, expression of C/EBPβ, and adipogenesis. When subjected to the standard adipocyte differentiation protocol, wild-type MEFs differentiate into adipocytes at high frequency, whereas CREB(-/-) MEFs exhibit greatly reduced expression of C/EBPβ and differentiation. The low level of expression of C/EBPβ and differentiation in CREB(-/-) MEFs appears to be due to up-regulation of other CREB protein family members, i.e. ATF1 and CREM.
Persistent Identifierhttp://hdl.handle.net/10722/180722
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, JWen_US
dc.contributor.authorKlemm, DJen_US
dc.contributor.authorVinson, Cen_US
dc.contributor.authorLane, MDen_US
dc.date.accessioned2013-01-28T01:41:58Z-
dc.date.available2013-01-28T01:41:58Z-
dc.date.issued2004en_US
dc.identifier.citationJournal Of Biological Chemistry, 2004, v. 279 n. 6, p. 4471-4478en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10722/180722-
dc.description.abstractThe proximal promoter of the C/EBPβ gene possesses dual cis regulatory elements (TGA1 and TGA2), both of which contain core CREB binding sites. Comparison of the activities of C/EBPβ promoter-reporter genes with 5′-truncations or site-directed mutations in the TGA elements showed that both are required for maximal promoter function. Electrophoretic mobility shift and chromatin immunoprecipitation (ChIP) analyses with antibodies specific to CREB and ATF1 showed that these CREB family members associate with the proximal promoter both in vitro and ex vivo. Immunoblotting and ChIP analysis revealed that other CREB family members, CREM and ATF1, are up-regulated and associate with the proximal C/EBPβ promoter in mouse embryonic fibroblasts (MEFs) from CREB(-/-) mice. ChIP analysis of wild-type MEFs and 3T3-L1 preadipocytes revealed that interaction of phospho-CREB, the active form of CREB, with the C/EBPβ gene promoter occurs only after induction of differentiation of 3T3-L1 preadipocytes and MEFs. Consistent with the interaction of CREB and ATF1 at the TGA regulatory elements, expression of constitutively active CREB strongly activated C/EBPβ promoter-reporter genes, induced expression of endogenous C/EBPβ, and caused adipogenesis in the absence of the hormonal inducers normally required. Conversely, expression of a dominant-negative CREB blocked promoter-reporter activity, expression of C/EBPβ, and adipogenesis. When subjected to the standard adipocyte differentiation protocol, wild-type MEFs differentiate into adipocytes at high frequency, whereas CREB(-/-) MEFs exhibit greatly reduced expression of C/EBPβ and differentiation. The low level of expression of C/EBPβ and differentiation in CREB(-/-) MEFs appears to be due to up-regulation of other CREB protein family members, i.e. ATF1 and CREM.en_US
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_US
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.subject.mesh3T3-L1 Cellsen_US
dc.subject.meshActivating Transcription Factor 1en_US
dc.subject.meshAdipocytes - Cytology - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCcaat-Enhancer-Binding Protein-Beta - Chemistry - Genetics - Metabolismen_US
dc.subject.meshCell Differentiationen_US
dc.subject.meshCyclic Amp Response Element-Binding Protein - Genetics - Metabolismen_US
dc.subject.meshDna, Complementary - Geneticsen_US
dc.subject.meshDna-Binding Proteinsen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshMutagenesis, Site-Directeden_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshRecombinant Proteins - Chemistry - Genetics - Metabolismen_US
dc.subject.meshTranscription Factors - Genetics - Metabolismen_US
dc.titleRole of CREB in Transcriptional Regulation of CCAAT/Enhancer-binding Protein β Gene during Adipogenesisen_US
dc.typeArticleen_US
dc.identifier.emailZhang, JW: jzhang1@hku.hken_US
dc.identifier.authorityZhang, JW=rp01713en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.M311327200en_US
dc.identifier.pmid14593102-
dc.identifier.scopuseid_2-s2.0-1042289760en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1042289760&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume279en_US
dc.identifier.issue6en_US
dc.identifier.spage4471en_US
dc.identifier.epage4478en_US
dc.identifier.isiWOS:000188554300067-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridZhang, JW=7601339417en_US
dc.identifier.scopusauthoridKlemm, DJ=7102294864en_US
dc.identifier.scopusauthoridVinson, C=7004968265en_US
dc.identifier.scopusauthoridLane, MD=7401977437en_US

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