Gene interactions and pathways from curated databases and text-mining

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CDH1 — RAC1

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Kovacs et al., J Biol Chem 2002 : In this study, we used a functional cadherin ligand ( hE/Fc ) to directly test whether E-cadherin ligation regulates phosphatidylinositol 3-kinase ( PI 3-kinase ) and Rac signaling ... We report that homophilic cadherin ligation recruits Rac to nascent adhesive contacts and specifically stimulates Rac signaling
Goodwin et al., J Biol Chem 2003 : Minimal mutation of the cytoplasmic tail inhibits the ability of E-cadherin to activate Rac but not phosphatidylinositol 3-kinase : direct evidence of a role for cadherin activated Rac signaling in adhesion and contact formation ... These data provide direct evidence for a role of cadherin activated Rac signaling in contact formation and adhesive stabilization
Honda et al., Genes Cells 2003 : Cdc42 or Rac was not essential for the association of nectin-1 and E-cadherin to form AJs
Noritake et al., Mol Biol Cell 2004 : The small guanosine triphosphatase Rac1 is activated by E-cadherin mediated cell-cell adhesion and is required for the accumulation of actin filaments, E-cadherin , and beta-catenin at sites of cell-cell contact ... Together, these results indicate that Rac1 enhances the accumulation of actin filaments, E-cadherin , and beta-catenin by acting on IQGAP1 and suggest that there exists a positive feedback loop comprised of "E-cadherin mediated cell-cell adhesion -- > Rac1 activation -- > actin-meshwork formation by IQGAP1 -- > increasing E-cadherin mediated cell-cell adhesion. ''
Hoshino et al., Mol Biol Cell 2004 : A novel role of nectins in inhibition of the E-cadherin induced activation of Rac and formation of cell-cell adherens junctions ... Moreover, we found here that the nectins, which did not trans-interact with other nectins ( non-trans interacting nectins ), inhibited the E-cadherin induced activation of Rac and reduced the velocity of the formation of the E-cadherin based cell-cell AJs ... These results indicate a novel role of nectins in regulation of the E-cadherin induced activation of Rac and formation of cell-cell AJs
Fukuyama et al., Oncogene 2006 : Activation of Rac by cadherin through the c-Src-Rap1-phosphatidylinositol 3-kinase-Vav2 pathway ... However, it has not fully been understood how cadherin induces the activation of Rac
Matsuda et al., J Mol Cell Cardiol 2006 : RhoA and Rac1 activation was inhibited by the transfection of dominant negative N-cadherin , indicating that RhoA and Rac1 were activated by N-cadherin in the oriented cardiac myocytes
Liu et al., J Cell Biol 2006 : Rac1 activity, which was induced by E-cadherin engagement specifically at intermediate seeding densities, was required for the cadherin stimulated proliferation, and the control of Rac1 activation by E-cadherin was mediated by p120-catenin
Kraemer et al., Am J Physiol Cell Physiol 2007 : We found that homophilic engagement of E-cadherin simultaneously activates both Rac1 and Cdc42 ... To pursue upstream elements of the Rac1 signaling pathway, we focused on the potential contribution of Tiam1 to cadherin activated Rac signaling
Esufali et al., Cancer Res 2007 (Colorectal Neoplasms) : Furthermore, we show that Rac1b negatively regulates E-cadherin expression and results in decreased adhesion of colorectal cancer cells
Perez et al., J Biol Chem 2008 : We propose that initial E-cadherin accumulation requires active membrane dynamics and involves diffusion mediated trapping at contact sites ; to propagate further contacts, phosphatidylinositol 3-kinase and Rac1 are transiently activated by E-cadherin engagement and initiate a new round of membrane dynamics, but they are subsequently suppressed at that site to allow maintenance of weak E-cadherin mediated adhesion
Sakisaka et al., Methods Mol Biol 2008 : The endocytosis of trans interacting E-cadherin was inhibited by Rac and Cdc42 small G proteins, which were activated by trans interacting E-cadherin
Kitt et al., PloS one 2011 : Inhibition of E-cadherin engagement with DECMA-1 Fab fragments or competitive binding of soluble E-cadherin, or nectin2alpha extracellular domain completely inhibited Rac1 activity
Hu et al., Tumour Biol 2012 (Liver Neoplasms...) : miR-143 expression significantly decreased mRNA and protein levels of GEF1, GEF2, and K-RAS genes ; lowered the constitutive activities of RhoA, Rac1 , and Cdc42 GTPases ; decreased the protein levels of MMP-2 and MMP-9 ; but significantly increased the protein level of E-cadherin