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CDH2 — RAC1

Pathways - manually collected, often from reviews:

• NCI Pathway Database N-cadherin signaling events: RAC1/GDP complex (RAC1) → N-cadherin/Ca2+/beta catenin-gamma catenin/alpha catenin/p120 catenin complex (CDH2-CTNNB1_JUP-CTNNA1-CTNND1) (modification, collaborate)
  Gavard et al., J Cell Sci 2004, El Sayegh et al., Mol Biol Cell 2005
  Evidence: mutant phenotype, assay
• NCI Pathway Database N-cadherin signaling events: RAC1-CDC42/GDP complex (RAC1_CDC42) → N-cadherin/Ca2+/beta catenin-gamma catenin/alpha catenin/p120 catenin complex (CDH2-CTNNB1_JUP-CTNNA1-CTNND1) (modification, collaborate)
  Meriane et al., Mol Biol Cell 2000, Charrasse et al., J Cell Biol 2002, Comunale et al., Biol Cell 2007
  Evidence: mutant phenotype, assay, other species

Text-mined interactions from Literome

Kovacs et al., J Biol Chem 2002 : 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
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
El Sayegh et al., Mol Biol Cell 2005 : We conclude that N-cadherin ligation induces Rac dependent cortactin recruitment and Fer dependent cortactin phosphorylation, which in turn promotes enhanced mobilization and interaction of surface expressed N-cadherin in contacting cells
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 ... 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
Shintani et al., Mol Biol Cell 2006 : Phosphoinositide-3 kinase-Rac1-c-Jun NH2-terminal kinase signaling mediates collagen I-induced cell scattering and up-regulation of N-cadherin expression in mouse mammary epithelial cells
Kraemer et al., Am J Physiol Cell Physiol 2007 : To pursue upstream elements of the Rac1 signaling pathway, we focused on the potential contribution of Tiam1 to cadherin activated Rac signaling
Woods et al., J Biol Chem 2007 : Inhibition of Rac1 resulted in a reduction in the number, size, and organization of cellular condensations and decreased expression of N-cadherin ... Overexpression of Rac1 resulted in an increase in N-cadherin expression levels
Adam et al., J Am Coll Cardiol 2010 (Atrial Fibrillation...) : In neonatal rat cardiomyocytes and fibroblasts, a specific small molecule inhibitor of Rac1 or simvastatin completely prevented the angiotensin II-induced up-regulation of CTGF, Cx43, and N-cadherin expression ... Angiotensin II activates CTGF via activation of Rac1 and nicotinamide adenine dinucleotide phosphate oxidase, leading to up-regulation of Cx43, N-cadherin , and interstitial fibrosis and therefore contributing to the signal transduction of atrial structural remodeling
Theveneau et al., Dev Cell 2010 : At this cell contact, N-cadherin inhibits protrusion and Rac1 activity and in turn promotes protrusions and activation of Rac1 at the free edge