Gene interactions and pathways from curated databases and text-mining

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CTNND1 — EGF

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Hakak et al., Mol Cell Biol 1999 (MAP Kinase Signaling System) : A Cas mutant lacking the Src binding region did not potentiate the EGF response, suggesting that Cas enhances EGF signaling by binding to endogenous cellular Src or another Src family member
Wang et al., Oncogene 2000 (Bone Neoplasms...) : In contrast, LAR selectively inhibited the epidermal growth factor (EGF) induced phosphorylation of p130CAS and the formation of the complex between p130CAS and GRB2 but this effect did not influence the activation of MAPK by EGF
Keilhack et al., J Biol Chem 2000 : Different p120(ctn) isoforms expressed in human embryonal kidney 293 cells, exhibited differential binding to SHP-1 that correlated partly with the extent of EGF dependent p120(ctn) tyrosine phosphorylation
Ojaniemi et al., J Biol Chem 1997 : At low, mitogenic concentrations ( < 10 ng/ml ), EGF treatment induced a rapid and transient tyrosine phosphorylation of Cas and promoted the formation of a Cas-adapter protein Crk complex in intact cells. The increase in tyrosine phosphorylation of Cas paralleled an increase in the cellular content of actin stress fibers and occurred via a pathway that depended on the integrity of the cytoskeleton. Further, phosphatidylinositol 3'-kinase activity was found to be required for the EGF stimulated Cas phosphorylation and actin polymerization. At high concentrations ( > 30 ng/ml ), EGF treatment resulted in the tyrosine dephosphorylation of Cas in a time dependent manner with a concomitant decrease in the length and number of actin stress fibers
Dolfi et al., Proc Natl Acad Sci U S A 1998 : A dominant negative form of Cas in turn blocked the integrin-, but not epidermal growth factor - nor v-Src mediated JNK activation