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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
27
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pubmed:dateCreated |
2004-6-28
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pubmed:abstractText |
CCAAT/enhancer-binding protein beta (C/EBPbeta) is a member of the bZIP family of transcription factors that contribute to the regulation of a wide range of important cellular processes. The data in the present study document that transcription from the human C/EBPbeta gene is induced in response to endoplasmic reticulum stress, such as glucose deprivation, or treatment of cells with tunicamycin or thapsigargin. Transient transfection of C/EBPbeta genomic fragments linked to a luciferase reporter gene demonstrated that the C/EBPbeta promoter plays no major regulatory role. Instead, by deletion analysis it was discovered that a 46-bp region, located at a genomic site that corresponds to the 3'-untranslated region of the C/EBPbeta mRNA, harbored an element that was required for the stress response. Mutagenesis demonstrated that a cis-regulatory element located at nt +1614-1621 (5'-TGACGCAA-3') is responsible for activation of the C/EBPbeta gene. Electrophoresis mobility shift analysis revealed that proteins are bound to this element and that the amount of binding is increased following glucose deprivation. This element is homologous to a previously reported mammalian unfolded protein response element that binds XBP-1. Consistent with those data, overexpression of XBP-1 caused an increase in transcription that was mediated by the C/EBPbeta mammalian unfolded protein response element.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0021-9258
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
2
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pubmed:volume |
279
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
27948-56
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:15102854-Base Sequence,
pubmed-meshheading:15102854-Binding Sites,
pubmed-meshheading:15102854-Blotting, Northern,
pubmed-meshheading:15102854-CCAAT-Enhancer-Binding Protein-beta,
pubmed-meshheading:15102854-Cell Line,
pubmed-meshheading:15102854-Cell Line, Tumor,
pubmed-meshheading:15102854-Cell Nucleus,
pubmed-meshheading:15102854-Endoplasmic Reticulum,
pubmed-meshheading:15102854-Gene Deletion,
pubmed-meshheading:15102854-Gene Expression Regulation,
pubmed-meshheading:15102854-Genes, Reporter,
pubmed-meshheading:15102854-Glucose,
pubmed-meshheading:15102854-Humans,
pubmed-meshheading:15102854-Immunoblotting,
pubmed-meshheading:15102854-Luciferases,
pubmed-meshheading:15102854-Models, Genetic,
pubmed-meshheading:15102854-Molecular Sequence Data,
pubmed-meshheading:15102854-Mutagenesis, Site-Directed,
pubmed-meshheading:15102854-Protein Folding,
pubmed-meshheading:15102854-RNA, Messenger,
pubmed-meshheading:15102854-Response Elements,
pubmed-meshheading:15102854-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:15102854-Thapsigargin,
pubmed-meshheading:15102854-Time Factors,
pubmed-meshheading:15102854-Transcription, Genetic,
pubmed-meshheading:15102854-Transcription Factors,
pubmed-meshheading:15102854-Transcriptional Activation,
pubmed-meshheading:15102854-Transfection,
pubmed-meshheading:15102854-Tunicamycin
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pubmed:year |
2004
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pubmed:articleTitle |
Human CCAAT/enhancer-binding protein beta gene expression is activated by endoplasmic reticulum stress through an unfolded protein response element downstream of the protein coding sequence.
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pubmed:affiliation |
Department of Biochemistry and Molecular Biology, Center for Mammalian Genetics, and Center for Nutritional Sciences, University of Florida College of Medicine, Gainesville, FL 32610-0245, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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