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Involvement of heterophilic trans ‐interaction of Necl‐5/Tage4/PVR/CD155 with nectin‐3 in formation of nectin‐ and cadherin‐based adherens junctions
Author(s) -
Sato Tatsuhiro,
Irie Kenji,
Ooshio Takako,
Ikeda Wataru,
Takai Yoshimi
Publication year - 2004
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2004.00763.x
Subject(s) - nectin , adherens junction , cadherin , biology , cell adhesion molecule , microbiology and biotechnology , catenin , cell adhesion , cell–cell interaction , cell , signal transduction , biochemistry , wnt signaling pathway
Nectins, Ca 2+ ‐independent immunoglobulin (Ig)‐like cell–cell adhesion molecules and cadherins, Ca 2+ ‐dependent cell–cell adhesion molecules, are associated through their respective cytoplasmic tail‐binding proteins, afadin and catenins and play roles in formation of adherens junctions (AJs) in epithelial cells and fibroblasts. Nectin‐like molecule‐5 (Necl‐5) is a Ca 2+ ‐independent Ig‐like molecule which does not homophilically trans ‐interact, but heterophilically trans‐ interacts with nectin‐3, one member of the nectin family. Necl‐5 does not directly bind afadin and therefore is not associated with cadherins. Necl‐5 regulates cell motility and proliferation in cooperation with integrins and growth factor receptors, when it does not interact with nectin‐3. We studied here a role of the heterophilic trans ‐interaction of Necl‐5 with nectin‐3 in cell–cell adhesion using L cells stably expressing Necl‐5, nectin‐3 and E‐cadherin (Necl‐5‐nectin‐3‐EL cells). Afadin, E‐cadherin and catenins were recruited to the nectin‐3 side, but not to the Necl‐5 side, of the contact sites formed by the heterophilic trans ‐interaction between Necl‐5 and nectin‐3. The anti‐Necl‐5 monoclonal antibody, which specifically inhibited the heterophilic trans ‐interaction of Necl‐5 with nectin‐3, inhibited the formation of the E‐cadherin‐based AJs in Necl‐5‐nectin‐3‐EL cells. These results indicate that Necl‐5 plays roles not only in cell motility and proliferation but also in cell–cell adhesion in cooperation with nectin‐3.