Gene interactions and pathways from curated databases and text-mining

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EGF — MTOR

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Zhong et al., Biochem Biophys Res Commun 2001 (Prostatic Neoplasms) : Compared to that of HIF-1alpha, the constitutive, serum-, EGF- , and PMA increased HIF-1beta protein expression were also inhibited by selective PI3K or FRAP/TOR inhibitors but in higher doses
Galbaugh et al., BMC cell biology 2006 : The EGF induced activation of PI-3-kinase-Akt-mTOR regulates phosphorylation of molecules including ribosomal protein S6, eIF4E and 4E-BP1 that influence translational control in HC11 cells undergoing lactogenic differentiation
Sobolewska et al., Eur J Cell Biol 2009 : We also show that IGF-I and EGF are involved in the activation of mTOR in bovine MEC, whereas inhibition of mTOR by rapamycin abrogated the suppressive effects of IGF-I and EGF on autophagy
Codeluppi et al., J Neurosci 2009 (Disease Models, Animal...) : Indeed, we found that Rheb is required for EGF dependent mTOR activation in spinal cord astrocytes, whereas the Ras-MAP kinase pathway does not appear to be involved
Kramer et al., J Appl Physiol 2011 (Airway Remodeling...) : Thus rapamycin reduced airway remodeling and AHR, demonstrating an important role for mTOR signaling in TGF-a-induced/EGF receptor mediated reactive airway disease
Díaz et al., Cell Signal 2012 : While Akt expression was increased in GH-overexpressing mice, EGF induced phosphorylation of Akt, relative to its protein content, was diminished at Ser473 and inhibited at Thr308 ; consequently, mTOR , which is a substrate of Akt, was not activated by EGF
Xu et al., J Biol Chem 2012 : Bafilomycin, an inhibitor of V-ATPase, inhibited EGF stimulated DNA synthesis and mammalian target of rapamycin complex 1 ( mTORC1 ) activation as indicated by a decrease in eukaryotic initiation factor 4E-binding 1 ( 4E-BP1 ) phosphorylation and p70 ribosomal S6 protein kinase (p70S6K) phosphorylation and kinase activity ... Cycloheximide, a translation elongation inhibitor known to augment intracellular amino acid levels, prevented the effect of bafilomycin on amino acids levels and completely reversed its inhibition of EGF induced mTORC1 activation
Cornez et al., J Neurooncol 2013 (Brain Neoplasms...) : EGF signalling and rapamycin mediated mTOR inhibition in glioblastoma multiforme evaluated by phospho-specific flow cytometry
Haslinger et al., Biol Reprod 2013 : Accordingly, a decrease in EGF stimulated phosphorylation of AKT ( Ser473 and Thr308 ) and its downstream target mTORC1 ( Ser2448 ) was noticed in AKT1 and AKT3 shRNAmir cell pools