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dc.contributor.authorWan, Hen_US
dc.contributor.authorLin, Ken_US
dc.contributor.authorTsang, SMen_US
dc.contributor.authorUttagomol, Jen_US
dc.description.abstractThis 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.en_US
dc.format.extent124 - 134en_US
dc.relation.ispartofData Briefen_US
dc.subjectSequence alignmenten_US
dc.subjectSrc signalingen_US
dc.titleEvidence for Dsg3 in regulating Src signaling by competing with it for binding to caveolin-1.en_US
dc.rights.holder© 2016 The Authors
pubs.notesNot knownen_US
pubs.publication-statusPublished onlineen_US

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