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CTNND1 — EGF
Pathways - manually collected, often from reviews:
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OpenBEL Selventa BEL large corpus:
CTNND1
→
EGF
(increases)
Olsen et al., Cell 2006*
Evidence: We have detected 6,600 phosphorylation sites on 2,244 proteins and have determined their temporal dynamics after stimulating HeLa cells with epidermal growth factor (EGF) and recorded them in the Phosida database
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NCI Pathway Database Posttranslational regulation of adherens junction stability and dissassembly:
EGFR/EGFR/EGF/EGF complex (EGFR-EGF)
→
E-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1-CTNNA1-CTNND1)
(modification, activates)
Miravet et al., Mol Cell Biol 2003, Hoschuetzky et al., J Cell Biol 1994, Shibamoto et al., Cell adhesion and communication 1994
Evidence: assay, physical interaction
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NCI Pathway Database Stabilization and expansion of the E-cadherin adherens junction:
EGF (EGF)
→
E-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1-CTNNA1-CTNND1)
(modification, collaborate)
Qian et al., EMBO J 2004, Hoschuetzky et al., J Cell Biol 1994, Takahashi et al., Exp Cell Res 1996
Evidence: assay, physical interaction
-
NCI Pathway Database Stabilization and expansion of the E-cadherin adherens junction:
E-cadherin/Ca2+/beta catenin/alpha catenin/p120 catenin complex (CDH1-CTNNB1-CTNNA1-CTNND1)
→
EGFR/EGFR/EGF/EGF complex (EGFR-EGF)
(modification, inhibits)
Qian et al., EMBO J 2004, Hoschuetzky et al., J Cell Biol 1994, Takahashi et al., Exp Cell Res 1996
Evidence: assay, physical interaction
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