Gene interactions and pathways from curated databases and text-mining

◀ Back to EPHB2

EPHB2 — WNT3A

Text-mined interactions from Literome

Yun et al., J Cell Sci 2005 : Wnt3a induced ERK activation was maintained even though basal ERK activities were reduced by beta-catenin siRNA, indicating that Wnt3a may activate the ERK pathway independently of beta-catenin
Almeida et al., J Biol Chem 2005 : Wnt3a increased the expression of the anti-apoptotic protein Bcl-2 in an ERK dependent manner
Kim et al., Cell Signal 2007 : The RAF-1 -- > MEK -- > ERK cascade was immediately increased by WNT3a treatment, however, the upstream event triggering ERK pathway activation by WNT3a is not clear ... WNT3a activated RAS and WNT3a induced ERK activation was blocked by dominant negative RAS, indicating that WNT3a might act upstream of RAS ... WNT3a induced ERK pathway activations were blocked by AG1478, the epidermal growth factor receptor (EGFR) inhibitor, and EGFR siRNA ... The WNT3a induced ERK pathway activation was not observed in fibroblasts retaining defective EGFR, but the WNT3a effect was restored by EGFR reconstitution ... WNT3a induced ERK pathway activation was not affected by Dickkoff-1 (DKK-1), although WNT3a induced activations of the WNT/beta-catenin pathway and proliferation were reduced by DKK-1
Caverzasio et al., Endocrinology 2007 : In C3H10T1/2 mesenchymal cells, Wnt3a induced a rapid and transient activation of MAPKs p38 and ERK ... Dickkopf 1, a selective antagonist of Wnt proteins binding to low-density lipoprotein-receptor related protein-5/6 did not influence activation of p38 and ERK induced by Wnt3a ... In conclusion, Wnt3a activates ERK and p38 in mesenchymal C3H10T1/2 cells by a low-density lipoprotein-receptor related protein-5/6 independent mechanism
Halleskog et al., Cell Signal 2013 : Inhibition of heterotrimeric G proteins by pertussis toxin blocks WNT-3A induced LRP6 phosphorylation, disheveled shift, ß-catenin stabilization and phosphorylation of ERK1/2 ... WNT-3A induced ERK1/2 phosphorylation is mediated by ß? subunits, PLC, intracellular calcium and MEK1/2