Gene interactions and pathways from curated databases and text-mining

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EGF — RALA

Text-mined interactions from Literome

Nakashima et al., EMBO J 1999 : Taken together with the observation that EGF and insulin activate Ral , these results suggest that Ral, RalBP1 and POB1 transmit the signal from the receptors to Epsin and Eps15, thereby regulating ligand dependent receptor mediated endocytosis
Lu et al., Mol Cell Biol 2000 (Cell Transformation, Neoplastic) : In the EGFR cells, EGF induced a Ras dependent activation of RalA ... The activation of PLD by EGF in these cells was dependent upon both Ras and RalA ... Importantly, overexpression of wild-type RalA or an activated RalA mutant increased PLD activity in the absence of EGF and transformed the EGFR cells
Goi et al., EMBO J 2000 : These results identify a role for Ral-GTPases in the activation of c-Src by EGF receptors and the coupling of EGF to transcription through Stat3 and the actin cytoskeleton through cortactin
Gildea et al., Cancer Res 2002 (Neoplasm Metastasis...) : In addition, activation of RalA and expression of Rho were increased by EGF stimulation in both the nonmetastatic and metastatic variants of the same cell line
Tian et al., EMBO J 2002 : Previous work has demonstrated that epidermal growth factor (EGF) activates Ral-GEFs , at least in part, by a Ras mediated redistribution of the GEFs to their target, Ral-GTPases, in the plasma membrane ... Here we show that Ral-GEF stimulation by EGF involves an additional mechanism, PI3-K dependent kinase 1 (PDK1) induced enhancement of Ral-GEF catalytic activity
Yu et al., Oncogene 2002 (Breast Neoplasms) : In contrast, EGF receptors did require Ral activation to induce estrogen independent proliferation, while Ral activation was not required for estrogen induced proliferation of MCF-7 cells
Takaya et al., Mol Biol Cell 2004 : By using fluorescence resonance energy transfer based probes for RalA activity, we found that the EGF induced RalA activation in Cos7 cells was restricted at the EGF induced nascent lamellipodia, whereas under a similar condition both Ras activation and Ras dependent translocation of Ral GEFs occurred more diffusely at the plasma membrane ... This EGF induced RalA activation was not observed when lamellipodial protrusion was suppressed by a dominant negative mutant of Rac1, a GTPase activating protein for Cdc42, inhibitors of phosphatidylinositol 3-kinase, or inhibitors of actin polymerization
Barnes et al., PloS one 2010 (Atrophy...) : Our results indicate that ( i ) RAL induced in vitro and in vivo keratinocyte proliferation is a CD44 dependent phenomenon and requires the presence of HA, HB-EGF , erbB1 and MMPs, ( ii ) RAL and HAFi show a synergy in vitro and in vivo in mouse skin, and ( iii ) the combination of RAL and HAFi seems to have an important therapeutic effect in dermatoporosis
Kishida et al., Oncogene 1997 : Ral GDP dissociation stimulator (RalGDS), a putative effector protein of Ras, stimulated the GDP/GTP exchange reaction of the post-tanslationally lipid modified but not the unmodified form of Ral in response to epidermal growth factor in COS cells
Wolthuis et al., Curr Biol 1998 : This activation correlates with the activation of Ras, and dominant negative Ras completely inhibits Ral activation induced by insulin and epidermal growth factor (EGF)
Hofer et al., Curr Biol 1998 : Lysophosphatidic acid (LPA) and epidermal growth factor (EGF) , which activate both Ras dependent and Ras independent signaling pathways [ 10,11 ], rapidly activated Ral