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    Genomic organization and promoter cloning of the human X11α gene APBA1.

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    Authors
    Chai, Ka-Ho
    McLoughlin, Declan M
    Chan, Ting Fung
    Chan, Ho Yin Edwin
    Lau, Kwok-Fai
    Affiliation
    Biochemistry Program, School Life Sciences, The Chinese University of Hong Kong , Shatin, New Territories, Hong Kong SAR.
    Issue Date
    2012-05
    MeSH
    Adaptor Proteins, Signal Transducing
    Animals
    Base Sequence
    Blotting, Western
    Cells, Cultured
    Cerebral Cortex
    Cloning, Molecular
    Electrophoretic Mobility Shift Assay
    Enzyme-Linked Immunosorbent Assay
    Exons
    Genomics
    Humans
    Luciferases
    Molecular Sequence Data
    Nerve Tissue Proteins
    Neurons
    Promoter Regions, Genetic
    RNA, Messenger
    Rats
    Rats, Sprague-Dawley
    Real-Time Polymerase Chain Reaction
    Reverse Transcriptase Polymerase Chain Reaction
    Transcription Initiation Site
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    Citation
    Genomic organization and promoter cloning of the human X11α gene APBA1. 2012, 31 (5):651-9 DNA Cell Biol.
    Journal
    DNA and cell biology
    URI
    http://hdl.handle.net/10147/244221
    DOI
    10.1089/dna.2011.1447
    PubMed ID
    22136355
    Abstract
    X11α is a brain specific multi-modular protein that interacts with the Alzheimer's disease amyloid precursor protein (APP). Aggregation of amyloid-β peptide (Aβ), an APP cleavage product, is believed to be central to the pathogenesis of Alzheimer's disease. Recently, overexpression of X11α has been shown to reduce Aβ generation and to ameliorate memory deficit in a transgenic mouse model of Alzheimer's disease. Therefore, manipulating the expression level of X11α may provide a novel route for the treatment of Alzheimer's disease. Human X11α is encoded by the gene APBA1. As evidence suggests that X11α expression can be regulated at transcription level, we have determined the gene structure and cloned the promoter of APBA1. APBA1 spans over 244 kb on chromosome 9 and is composed of 13 exons and has multiple transcription start sites. A putative APBA1 promoter has been identified upstream of exon 1 and functional analysis revealed that this is highly active in neurons. By deletion analysis, the minimal promoter was found to be located between -224 and +14, a GC-rich region that contains a functional Sp3 binding site. In neurons, overexpression of Sp3 stimulates the APBA1 promoter while an Sp3 inhibitor suppresses the promoter activity. Moreover, inhibition of Sp3 reduces endogenous X11α expression and promotes the generation of Aβ. Our findings reveal that Sp3 play an essential role in APBA1 transcription.
    Item Type
    Article
    Language
    en
    ISSN
    1557-7430
    ae974a485f413a2113503eed53cd6c53
    10.1089/dna.2011.1447
    Scopus Count
    Collections
    St. Patrick's University Hospital

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