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dc.contributor.authorHao, Yan
dc.contributor.authorChai, Ka-Ho
dc.contributor.authorMcLoughlin, Declan M
dc.contributor.authorChan, Ho Yin Edwin
dc.contributor.authorLau, Kwok-Fai
dc.date.accessioned2012-09-17T08:42:59Z
dc.date.available2012-09-17T08:42:59Z
dc.date.issued2012-02-15
dc.identifier.citationPromoter characterization and genomic organization of the human X11β gene APBA2. 2012, 23 (3):146-51 Neuroreporten_GB
dc.identifier.issn1473-558X
dc.identifier.pmid22222501
dc.identifier.doi10.1097/WNR.0b013e32834f1934
dc.identifier.urihttp://hdl.handle.net/10147/244195
dc.description.abstractOverexpression of neuronal adaptor protein X11β has been shown to decrease the production of amyloid-β, a toxic peptide deposited in Alzheimer's disease brains. Therefore, manipulation of the X11β level may represent a potential therapeutic strategy for Alzheimer's disease. As X11β expression can be regulated at the transcription level, we determined the genomic organization and the promoter of the human X11β gene, amyloid β A4 precursor protein-binding family A member 2 (APBA2). By RNA ligase-mediated rapid amplification of cDNA ends, a single APBA2 transcription start site and the complete sequence of exon 1 were identified. The APBA2 promoter was located upstream of exon 1 and was more active in neurons. The core promoter contains several CpG dinucleotides, and was strongly suppressed by DNA methylation. In addition, mutagenesis analysis revealed a putative Pax5-binding site within the promoter. Together, APBA2 contains a potent neuronal promoter whose activity may be regulated by DNA methylation and Pax5.
dc.language.isoenen
dc.rightsArchived with thanks to Neuroreporten_GB
dc.subject.meshBase Sequence
dc.subject.meshBinding Sites
dc.subject.meshBrain
dc.subject.meshCadherins
dc.subject.meshCarrier Proteins
dc.subject.meshDNA Methylation
dc.subject.meshGene Expression Regulation
dc.subject.meshGenome, Human
dc.subject.meshHumans
dc.subject.meshMolecular Sequence Data
dc.subject.meshMutagenesis
dc.subject.meshNerve Tissue Proteins
dc.subject.meshPromoter Regions, Genetic
dc.subject.meshTranscription, Genetic
dc.titlePromoter characterization and genomic organization of the human X11β gene APBA2.en_GB
dc.typeArticleen
dc.contributor.departmentBiochemistry Program, School of Life Sciences, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR.en_GB
dc.identifier.journalNeuroreporten_GB
dc.description.provinceLeinsteren
html.description.abstractOverexpression of neuronal adaptor protein X11β has been shown to decrease the production of amyloid-β, a toxic peptide deposited in Alzheimer's disease brains. Therefore, manipulation of the X11β level may represent a potential therapeutic strategy for Alzheimer's disease. As X11β expression can be regulated at the transcription level, we determined the genomic organization and the promoter of the human X11β gene, amyloid β A4 precursor protein-binding family A member 2 (APBA2). By RNA ligase-mediated rapid amplification of cDNA ends, a single APBA2 transcription start site and the complete sequence of exon 1 were identified. The APBA2 promoter was located upstream of exon 1 and was more active in neurons. The core promoter contains several CpG dinucleotides, and was strongly suppressed by DNA methylation. In addition, mutagenesis analysis revealed a putative Pax5-binding site within the promoter. Together, APBA2 contains a potent neuronal promoter whose activity may be regulated by DNA methylation and Pax5.


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