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    A Mechanosensor Mechanism Controls the G-Quadruplex/i-Motif Molecular Switch in the MYC Promoter NHE III 1

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    Hurley_Mechanosensor.pdf
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    Description:
    Final Accepted Manuscript
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    Author
    Sutherland, Caleb
    Cui, Yunxi
    Mao, Hanbin
    Hurley, Laurence H.
    Affiliation
    University of Arizona Cancer Center
    University of Arizona, College of Pharmacy
    Issue Date
    2016-10-26
    
    Metadata
    Show full item record
    Publisher
    AMER CHEMICAL SOC
    Citation
    A Mechanosensor Mechanism Controls the G-Quadruplex/i-Motif Molecular Switch in the MYC Promoter NHE III 1 2016, 138 (42):14138 Journal of the American Chemical Society
    Journal
    Journal of the American Chemical Society
    Rights
    © 2016 American Chemical Society
    Collection Information
    This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.
    Abstract
    MYC is overexpressed in many different cancer types and is an intensively studied oncogene because of its contributions to tumorigenesis. The regulation of MYC is complex, and the NHE III1 and FUSE elements rely upon noncanonical DNA structures and transcriptionally induced negative superhelicity. In the NHE III1 only the G-quadruplex has been extensively studied, whereas the role of the i-motif, formed on the opposite C-rich strand, is much less understood. We demonstrate here that the i-motif is formed within the 4CT element and is recognized by hnRNP K, which leads to a low level of transcription activation. For maximal hnRNP K transcription activation, two additional cytosine runs, located seven bases downstream of the i-motif-forming region, are also required. To access these additional runs of cytosine, increased negative superhelicity is necessary, which leads to a thermodynamically stable complex between hnRNP K and the unfolded i-motif. We also demonstrate mutual exclusivity between the MYC G-quadruplex and i-motif, providing a rationale for a molecular switch mechanism driven by SP1-induced negative superhelicity, where relative hnRNP K and nucleolin expression shifts the equilibrium to the on or off state.
    Note
    12 month embargo. First available online 26 September 2016.
    ISSN
    0002-7863
    1520-5126
    DOI
    10.1021/jacs.6b09196
    Version
    Final accepted manuscript
    Sponsors
    National Science Foundation [CH-1609514, CHE-1415883]; National Institutes of Health [5R01CA153821, 1R01GM085585]; National Foundation for Cancer Research [VONHOFF-15-01]
    Additional Links
    http://pubs.acs.org/doi/abs/10.1021/jacs.6b09196
    ae974a485f413a2113503eed53cd6c53
    10.1021/jacs.6b09196
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