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    Transcriptional regulation of human FE65, a ligand of Alzheimer's disease amyloid precursor protein, by Sp1.

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    Authors
    Yu, Hoi-Tin
    Chan, William Wai-Lun
    Chai, Ka-Ho
    Lee, Chris Wing-Cheung
    Chang, Raymond Chuen-Chung
    Yu, Man-Shan
    McLoughlin, Declan M
    Miller, Christopher C J
    Lau, Kwok-Fai
    Affiliation
    Department of Biochemistry (Science), The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR.
    Issue Date
    2010-03-01
    MeSH
    Amyloid beta-Protein Precursor
    Gene Expression Regulation
    Humans
    Nerve Tissue Proteins
    Neurons
    Nuclear Proteins
    Promoter Regions, Genetic
    RNA, Messenger
    Sp1 Transcription Factor
    Transcription, Genetic
    
    Metadata
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    Citation
    Transcriptional regulation of human FE65, a ligand of Alzheimer's disease amyloid precursor protein, by Sp1. 2010, 109 (4):782-93 J. Cell. Biochem.
    Journal
    Journal of cellular biochemistry
    URI
    http://hdl.handle.net/10147/128732
    DOI
    10.1002/jcb.22457
    PubMed ID
    20091743
    Additional Links
    http://dx.doi.org/10.1002/jcb.22457
    Abstract
    FE65 is a neuronal-enriched adaptor protein that binds to the Alzheimer's disease amyloid precursor protein (APP). FE65 forms a transcriptionally active complex with the APP intracellular domain (AICD). The precise gene targets for this complex are unclear but several Alzheimer's disease-linked genes have been proposed. Additionally, evidence suggests that FE65 influences APP metabolism. The mechanism by which FE65 expression is regulated is as yet unknown. To gain insight into the regulatory mechanism, we cloned a 1.6 kb fragment upstream of the human FE65 gene and found that it possesses particularly strong promoter activity in neurones. To delineate essential regions in the human FE65 promoter, a series of deletion mutants were generated. The minimal FE65 promoter was located between -100 and +5, which contains a functional Sp1 site. Overexpression of the transcription factor Sp1 potentiates the FE65 promoter activity. Conversely, suppression of the FE65 promoter was observed in cells either treated with an Sp1 inhibitor or in which Sp1 was knocked down. Furthermore, reduced levels of Sp1 resulted in downregulation of endogenous FE65 mRNA and protein. These findings reveal that Sp1 plays a crucial role in transcriptional control of the human FE65 gene.
    Language
    en
    ISSN
    1097-4644
    ae974a485f413a2113503eed53cd6c53
    10.1002/jcb.22457
    Scopus Count
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