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E-cadherin and Hakai: signalling, remodeling or destruction?

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Activation of tyrosine kinase receptors in epithelial cells results in the rapid disassembly of E-cadherin-mediated cell–cell adhesions. New research has identified Hakai, an E3-ubiquitin-ligase related to Cbl that binds E-cadherin in a tyrosine phosphorylation-dependent manner. By promoting the endocytosis and dynamic recycling or destruction of E-cadherin complexes, Hakai may control epithelial–mesenchymal transitions under physiological and pathological conditions.

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Figure 1: A model for Hakai in the dynamic regulation of E-cadherin-mediated adherens junction.

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Authors and Affiliations

  1. Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research and National Institutes of Health, Bethesda, 20892-4330, Maryland, USA

    J. Silvio Gutkind

  2. Department of Experimental Oncology, European Institute of Oncology, Milan, 20141, Italy

    Salvatore Pece

Authors
  1. Salvatore Pece
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  2. J. Silvio Gutkind
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Pece, S., Gutkind, J. E-cadherin and Hakai: signalling, remodeling or destruction?. Nat Cell Biol 4, E72–E74 (2002). https://doi.org/10.1038/ncb0402-e72

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