@article{
 title = {All-trans retinoic acid down-regulates human albumin gene expression through the induction of C/EBPbeta-LIP.},
 type = {article},
 year = {2006},
 identifiers = {[object Object]},
 keywords = {Albumins,Albumins: biosynthesis,Albumins: genetics,Binding Sites,CCAAT-Enhancer-Binding Protein-beta,CCAAT-Enhancer-Binding Protein-beta: metabolism,Carcinoma, Hepatocellular,Carcinoma, Hepatocellular: genetics,Cell Line, Tumor,Down-Regulation,Gene Expression Regulation,Humans,Promoter Regions, Genetic,Protein Binding,Transcriptional Activation,Tretinoin,Tretinoin: physiology},
 pages = {345-53},
 volume = {397},
 websites = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1513275&tool=pmcentrez&rendertype=abstract},
 month = {7},
 day = {15},
 id = {4dc1bbb0-4eb7-35b1-8e2c-c83e3f97a680},
 created = {2016-04-08T12:19:26.000Z},
 accessed = {2015-03-24},
 file_attached = {true},
 profile_id = {994bc413-6766-31df-917a-32165aa30f6c},
 group_id = {cec5aa9e-65e1-3c21-bc44-78fa6504020e},
 last_modified = {2017-03-14T10:42:46.538Z},
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 hidden = {false},
 citation_key = {Masaki2006},
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 abstract = {ATRA (all-trans retinoic acid), which is a major bioactive metabolite of vitamin A and a potent regulator of development and differentiation, mediates down-regulation of the human albumin gene. However, the mechanism of ATRA-mediated down-regulation is not well understood. In the present study, deletion analysis and luciferase assays demonstrate that ATRA causes a marked decrease in the activity of the albumin promoter, the region between nt -367 and -167 from the transcription start site, where C/EBP (CCAAT/enhancer-binding protein)-binding sites are tightly packed, is indispensable for ATRA-mediated down-regulation. ChIP (chromatin immunoprecipitation) assays revealed that in vivo binding of C/EBPalpha to the region markedly decreases upon incubation with ATRA, whereas ATRA treatment marginally increases the recruitment of C/EBPbeta. We found that ATRA has the ability to differentially and directly induce expression of a truncated isoform of C/EBPbeta, which is an LIP (liver-enriched transcriptional inhibitory protein) that lacks a transactivation domain, and to increase the binding activity of C/EBPbeta-LIP to its response element. Overexpression of C/EBPbeta-LIP negatively regulates the endogenous expression of albumin, as well as the activity of the albumin promoter induced by C/EBP transactivators such as C/EBPalpha and full-length C/EBPbeta. In conclusion, we propose a novel model for down-regulation of the albumin gene, in which ATRA triggers an increase in the translation of C/EBPbeta-LIP that antagonizes C/EBP transactivators by interacting with their binding sites in the albumin promoter.},
 bibtype = {article},
 author = {Masaki, Takahiro and Matsuura, Tomokazu and Ohkawa, Kiyoshi and Miyamura, Tatsuo and Okazaki, Isao and Watanabe, Tetsu and Suzuki, Tetsuro},
 journal = {The Biochemical journal},
 number = {2}
}

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However, the mechanism of ATRA-mediated down-regulation is not well understood. In the present study, deletion analysis and luciferase assays demonstrate that ATRA causes a marked decrease in the activity of the albumin promoter, the region between nt -367 and -167 from the transcription start site, where C/EBP (CCAAT/enhancer-binding protein)-binding sites are tightly packed, is indispensable for ATRA-mediated down-regulation. ChIP (chromatin immunoprecipitation) assays revealed that in vivo binding of C/EBPalpha to the region markedly decreases upon incubation with ATRA, whereas ATRA treatment marginally increases the recruitment of C/EBPbeta. We found that ATRA has the ability to differentially and directly induce expression of a truncated isoform of C/EBPbeta, which is an LIP (liver-enriched transcriptional inhibitory protein) that lacks a transactivation domain, and to increase the binding activity of C/EBPbeta-LIP to its response element. Overexpression of C/EBPbeta-LIP negatively regulates the endogenous expression of albumin, as well as the activity of the albumin promoter induced by C/EBP transactivators such as C/EBPalpha and full-length C/EBPbeta. In conclusion, we propose a novel model for down-regulation of the albumin gene, in which ATRA triggers an increase in the translation of C/EBPbeta-LIP that antagonizes C/EBP transactivators by interacting with their binding sites in the albumin promoter.","bibtype":"article","author":"Masaki, Takahiro and Matsuura, Tomokazu and Ohkawa, Kiyoshi and Miyamura, Tatsuo and Okazaki, Isao and Watanabe, Tetsu and Suzuki, Tetsuro","journal":"The Biochemical journal","number":"2","bibtex":"@article{\n title = {All-trans retinoic acid down-regulates human albumin gene expression through the induction of C/EBPbeta-LIP.},\n type = {article},\n year = {2006},\n identifiers = {[object Object]},\n keywords = {Albumins,Albumins: biosynthesis,Albumins: genetics,Binding Sites,CCAAT-Enhancer-Binding Protein-beta,CCAAT-Enhancer-Binding Protein-beta: metabolism,Carcinoma, Hepatocellular,Carcinoma, Hepatocellular: genetics,Cell Line, Tumor,Down-Regulation,Gene Expression Regulation,Humans,Promoter Regions, Genetic,Protein Binding,Transcriptional Activation,Tretinoin,Tretinoin: physiology},\n pages = {345-53},\n volume = {397},\n websites = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1513275&tool=pmcentrez&rendertype=abstract},\n month = {7},\n day = {15},\n id = {4dc1bbb0-4eb7-35b1-8e2c-c83e3f97a680},\n created = {2016-04-08T12:19:26.000Z},\n accessed = {2015-03-24},\n file_attached = {true},\n profile_id = {994bc413-6766-31df-917a-32165aa30f6c},\n group_id = {cec5aa9e-65e1-3c21-bc44-78fa6504020e},\n last_modified = {2017-03-14T10:42:46.538Z},\n read = {true},\n starred = {false},\n authored = {false},\n confirmed = {true},\n hidden = {false},\n citation_key = {Masaki2006},\n folder_uuids = {37786225-e8d4-483b-be04-dfc97f200748},\n private_publication = {false},\n abstract = {ATRA (all-trans retinoic acid), which is a major bioactive metabolite of vitamin A and a potent regulator of development and differentiation, mediates down-regulation of the human albumin gene. 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