Hakai, an E3-ligase for E-cadherin, stabilizes δ-catenin through Src kinase.Hakai ubiquitinates and induces endocytosis of the E-cadherin complex; thus, modulating cell adhesion and regulating development of the epithelial-mesenchymal transition of metastasis.  Although several published data show the interactions between δ-catenin and E-cadherin and between Hakai and E-cadherin separately, we found no published report on the relationship between δ-catenin and Hakai.  In this report, we show Hakai stabilizes δ-catenin regardless of its E3 ligase activity.  We show that Hakai and Src increase the stability of δ-catenin synergistically.  Hakai stabilizes Src and Src, which in turn, inhibits binding between glycogen synthase kinase-3β and δ-catenin, resulting in less proteosomal degradation of δ-catenin.  These results suggest that stabilization of δ-catenin by Hakai is dependent on Src.
Hakai
Hakai, an E3-ligase for E-cadherin, stabilizes δ-catenin through Src kinase.Hakai ubiquitinates and induces endocytosis of the E-cadherin complex; thus, modulating cell adhesion and regulating development of the epithelial-mesenchymal transition of metastasis.  Our previous published data show that δ-catenin promotes E-cadherin processing and thereby activates β-catenin-mediated oncogenic signals.  Although several published data show the interactions between δ-catenin and E-cadherin and between Hakai and E-cadherin separately, we found no published report on the relationship between δ-catenin and Hakai. 
E-cadherin
Hakai, an E3-ligase for E-cadherin, stabilizes δ-catenin through Src kinase.Hakai ubiquitinates and induces endocytosis of the E-cadherin complex; thus, modulating cell adhesion and regulating development of the epithelial-mesenchymal transition of metastasis. 
Src kinase