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PLoS One. 2010 Dec 3;5(12):e14211. doi: 10.1371/journal.pone.0014211.

Desmoglein 3, via an interaction with E-cadherin, is associated with activation of Src.

Author information

1
Centre for Clinical and Diagnostic Oral Sciences, Institute of Dentistry, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, London, United Kingdom.

Abstract

BACKGROUND:

Desmoglein 3 (Dsg3), a desmosomal adhesion protein, is expressed in basal and immediate suprabasal layers of skin and across the entire stratified squamous epithelium of oral mucosa. However, increasing evidence suggests that the role of Dsg3 may involve more than just cell-cell adhesion.

METHODOLOGY/PRINCIPAL FINDINGS:

To determine possible additional roles of Dsg3 during epithelial cell adhesion we used overexpression of full-length human Dsg3 cDNA, and RNAi-mediated knockdown of this molecule in various epithelial cell types. Overexpression of Dsg3 resulted in a reduced level of E-cadherin but a colocalisation with the E-cadherin-catenin complex of the adherens junctions. Concomitantly these transfected cells exhibited marked migratory capacity and the formation of filopodial protrusions. These latter events are consistent with Src activation and, indeed, Src-specific inhibition reversed these phenotypes. Moreover Dsg3 knockdown, which also reversed the decreased level of E-cadherin, partially blocked Src phosphorylation.

CONCLUSIONS/SIGNIFICANCE:

Our data are consistent with the possibility that Dsg3, as an up-stream regulator of Src activity, helps regulate adherens junction formation.

PMID:
21151980
PMCID:
PMC2997060
DOI:
10.1371/journal.pone.0014211
[Indexed for MEDLINE]
Free PMC Article
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