Reggies/flotillins regulate E-cadherin-mediated cell contact formation by affecting EGFR trafficking.

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Auteurs
Date

2012

Type de document
Périmètre
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Source

Serveur académique Lausannois

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Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1091/mbc.E11-12-1006

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/22438585

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1939-4586

Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_98D27A94BA194

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Serveur Académique Lausannois

Organisation

Université de Lausanne et CHUV

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info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer

Mots-clés 0

Adherens Junctions/metabolism; Adherens Junctions/ultrastructure; Cadherins/metabolism; Cell Adhesion; Cell Line, Tumor; Cell Movement; Endocytosis; Gene Knockdown Techniques; Humans; Membrane Proteins/genetics; Membrane Proteins/metabolism; Phosphoproteins/metabolism; Phosphorylation; Prions/genetics; Prions/metabolism; Protein Processing, Post-Translational; Protein Transport; RNA Interference; Receptor, Epidermal Growth Factor/metabolism; Signal Transduction; beta Catenin/metabolism

Sujets proches En

Adherence, Cell Cell adherence

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G.P. Solis et al., « Reggies/flotillins regulate E-cadherin-mediated cell contact formation by affecting EGFR trafficking. », Serveur académique Lausannois, ID : 10.1091/mbc.E11-12-1006

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The reggie/flotillin proteins are implicated in membrane trafficking and, together with the cellular prion protein (PrP), in the recruitment of E-cadherin to cell contact sites. Here, we demonstrate that reggies, as well as PrP down-regulation, in epithelial A431 cells cause overlapping processes and abnormal formation of adherens junctions (AJs). This defect in cell adhesion results from reggie effects on Src tyrosine kinases and epidermal growth factor receptor (EGFR): loss of reggies reduces Src activation and EGFR phosphorylation at residues targeted by Src and c-cbl and leads to increased surface exposure of EGFR by blocking its internalization. The prolonged EGFR signaling at the plasma membrane enhances cell motility and macropinocytosis, by which junction-associated E-cadherin is internalized and recycled back to AJs. Accordingly, blockage of EGFR signaling or macropinocytosis in reggie-deficient cells restores normal AJ formation. Thus, by promoting EGFR internalization, reggies restrict the EGFR signaling involved in E-cadherin macropinocytosis and recycling and regulate AJ formation and dynamics and thereby cell adhesion.

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