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    Evidence for Dsg3 in regulating Src signaling by competing with it for binding to caveolin-1. 
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    • Evidence for Dsg3 in regulating Src signaling by competing with it for binding to caveolin-1.
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    • Centre for Oral Immunobiology and Regenerative Medicine
    • Evidence for Dsg3 in regulating Src signaling by competing with it for binding to caveolin-1.
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    Evidence for Dsg3 in regulating Src signaling by competing with it for binding to caveolin-1.

    Volume
    6
    Pagination
    124 - 134
    DOI
    10.1016/j.dib.2015.11.049
    Journal
    Data Brief
    ISSN
    2352-3409
    Metadata
    Show full item record
    Abstract
    This data article contains extended, complementary analysis related to the research articles entitled "Desmoglein 3, via an interaction with E-cadherin, is associated with activation of Src" (Tsang et al., 2010) [1] and figures related to the review article entitled "Desmoglein 3: a help or a hindrance in cancer progression?" (Brown et al., 2014) [2]. We show here that both Src and caveolin-1 (Cav-1) associate with Dsg3 in a non-ionic detergent soluble pool and that modulation of Dsg3 levels inversely alters the expression of Src in the Cav-1 complex. Furthermore, immunofluorescence analysis revealed a reduced colocalization of Cav-1/total Src in cells with overexpression of Dsg3 compared to control cells. In support, the sequence analysis has identified a region within the carboxyl-terminus of human Dsg3 for a likelihood of binding to the scaffolding domain of Cav-1, the known Src binding site in Cav-1, and this region is highly conserved across most of 18 species as well as within desmoglein family members. Based on these findings, we propose a working model that Dsg3 activates Src through competing with its inactive form for binding to Cav-1, thus leading to release of Src followed by its auto-activation.
    Authors
    Wan, H; Lin, K; Tsang, SM; Uttagomol, J
    URI
    http://qmro.qmul.ac.uk/xmlui/handle/123456789/12355
    Collections
    • Centre for Oral Immunobiology and Regenerative Medicine [451]
    Language
    eng
    Licence information
    CC-BY
    Copyright statements
    © 2016 The Authors
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