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Nature Cell Biology 4, E72 - E74 (2002)
doi:10.1038/ncb0402-e72

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

Salvatore Pece2 & J. Silvio Gutkind1

  1. J. Silvio Gutkind is in the Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research and National Institutes of Health, Bethesda, Maryland 20892-4330, USA
    e-mail: sg39v@nih.gov
  2. Salvatore Pece is in the Department of Experimental Oncology, European Institute of Oncology, 20141 Milan, Italy

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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RESEARCH
Hakai, a c-Cbl-like protein, ubiquitinates and induces endocytosis of the E-cadherin complex
Nature Cell Biology Article (01 Mar 2002)

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