Key result
CAR regulates epithelial cell junction stability by destabilizing E-cadherin at cell-cell junctions and promoting its endocytosis through a Src- and PKCδ-dependent mechanism.
CAR regulates epithelial cell junction stability by promoting Src-dependent endocytosis of E-cadherin following phosphorylation by PKCδ.
CAR modulation of epithelial junctions may affect cardiac barrier integrity; leaves open therapeutic targeting pending human validation.
CAR (Coxsackie and Adenovirus Receptor) is the primary docking receptor for typeB coxsackie viruses and subgroup C adenoviruses. CAR is a member of the JAM family of adhesion receptors and is located to both tight and adherens junctions between epithelial cells where it can assemble adhesive contacts through homodimerisation in trans. However, the role of CAR in controlling epithelial junction dynamics remains poorly understood. Here we demonstrate that levels of CAR in human epithelial cells play a key role in determining epithelial cell adhesion through control of E-cadherin stability at cell-cell junctions. Mechanistically, we show that CAR is phosphorylated within the C-terminus by PKCδ and that this in turn controls Src-dependent endocytosis of E-cadherin at cell junctions. This data demonstrates a novel role for CAR in regulating epithelial homeostasis.
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Morton et al. (2013) studied Epithelial cell junction stability. CAR overexpression vs. Wild-type cells was evaluated on E-cadherin stability at cell-cell junctions. CAR regulates epithelial cell junction stability by destabilizing E-cadherin at cell-cell junctions and promoting its endocytosis through a Src- and PKCδ-dependent mechanism.
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