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    XBP1 activates the transcription of its target genes via an ACGT core sequence under ER stress

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    Authors
    Kanemoto, Soshi
    Kondo, Shinichi
    Ogata, Maiko
    Murakami, Tomohiko
    Urano, Fumihiko
    Imaizumi, Kazunori
    UMass Chan Affiliations
    Program in Molecular Medicine
    Program in Gene Function and Expression
    Document Type
    Journal Article
    Publication Date
    2005-05-11
    Keywords
    Base Sequence
    DNA
    DNA-Binding Proteins
    Endoplasmic Reticulum
    Hela Cells
    Humans
    Molecular Sequence Data
    Nuclear Proteins
    Promoter Regions, Genetic
    Transcription Factors
    Transcription, Genetic
    Genetics and Genomics
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    Link to Full Text
    http://dx.doi.org/10.1016/j.bbrc.2005.04.039
    Abstract
    In mammals, the transmembrane protein kinase/endoribonuclease IRE1 is activated by endoplasmic reticulum stress and subsequently processes XBP1 mRNA to generate an active form of XBP1 protein. The spliced form of XBP1 protein acts as a transcription factor and induces the expression of ER-resident molecular chaperones. However, the mechanism for how XBP1 promotes the transcription of its target genes as well as the cis-acting elements for XBP1 during ER stress has been unclear. Recently, it was demonstrated that the expression of MDG1/ERdj4, a member of the DnaJ family, is regulated by the IRE1-XBP1 pathway. In the present report, we investigated the regulatory mechanisms of MDG1/ERdj4 gene expression by XBP1. We identified a cis-acting element in the MDG1/ERdj4 promoter region, to which XBP1 specifically binds in response to ER stress. Our results reveal a target sequence for the IRE1-XBP1 pathway under ER stress conditions.
    Source
    Biochem Biophys Res Commun. 2005 Jun 17;331(4):1146-53. Link to article on publisher's site
    DOI
    10.1016/j.bbrc.2005.04.039
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/43919
    PubMed ID
    15882996
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.bbrc.2005.04.039
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