Linked Life Data

14593102

Source:http://linkedlifedata.com/resource/pubmed/id/14593102

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-2-2
pubmed:abstractText
The proximal promoter of the C/EBPbeta gene possesses dual cis regulatory elements (TGA1 and TGA2), both of which contain core CREB binding sites. Comparison of the activities of C/EBPbeta 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/EBPbeta 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/EBPbeta 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/EBPbeta promoter-reporter genes, induced expression of endogenous C/EBPbeta, 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/EBPbeta, 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/EBPbeta and differentiation. The low level of expression of C/EBPbeta and differentiation in CREB(-/-) MEFs appears to be due to up-regulation of other CREB protein family members, i.e. ATF1 and CREM.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
279
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4471-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:14593102-3T3-L1 Cells, pubmed-meshheading:14593102-Activating Transcription Factor 1, pubmed-meshheading:14593102-Adipocytes, pubmed-meshheading:14593102-Animals, pubmed-meshheading:14593102-Base Sequence, pubmed-meshheading:14593102-CCAAT-Enhancer-Binding Protein-beta, pubmed-meshheading:14593102-Cell Differentiation, pubmed-meshheading:14593102-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:14593102-DNA, Complementary, pubmed-meshheading:14593102-DNA-Binding Proteins, pubmed-meshheading:14593102-Gene Expression Regulation, pubmed-meshheading:14593102-Mice, pubmed-meshheading:14593102-Mice, Knockout, pubmed-meshheading:14593102-Mutagenesis, Site-Directed, pubmed-meshheading:14593102-Promoter Regions, Genetic, pubmed-meshheading:14593102-Recombinant Proteins, pubmed-meshheading:14593102-Transcription Factors
pubmed:year
2004
pubmed:articleTitle
Role of CREB in transcriptional regulation of CCAAT/enhancer-binding protein beta gene during adipogenesis.
pubmed:affiliation
Department of Biological Chemistry and Biochemistry, Cellular and Molecular Biology Program, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.