Gene interactions and pathways from curated databases and text-mining

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EIF4E — PI3

Text-mined interactions from Literome

Rao et al., J Biol Chem 1999 : These findings demonstrate that 1 ) PI3-kinase dependent and independent mechanisms appear to be involved in PGF2alpha induced activation of ERK2 ; 2 ) PGF2alpha induced eIF4E and 4E-BP1 phosphorylation appear to be mediated by both ERK dependent and PI3-kinase dependent rapamycin-sensitive mechanisms ; and 3 ) ERK dependent eIF4E phosphorylation but not PI3-kinase dependent p70 ( S6k ) activation correlates with PGF2alpha induced global protein synthesis and bFGF-2 expression in VSMC
Morley et al., Cell Signal 2003 : However, a cell-permeable, specific inhibitor of Mnk1, CGP57380 and the phosphatidylinositol-3-kinase (PI3-K) inhibitor, LY294002, prevented eIF4E phosphorylation in 293 cells irrespective of SAPK2a expression
Prasad et al., Oncogene 2009 (Lymphoma, Mantle-Cell) : Notably, ON 01910.Na suppressed eukaryotic translation initiation factor 4E ( eIF4E ) -mediated cyclin D1 mRNA translation, decreased levels of phosphorylated Akt, mammalian target of Rapamycin (mTOR) and eIF4E binding protein (eIF4E-BP), lowered the cap site binding activity of eIF4E and directly inhibited activity of phosphatidylinositol-3 kinase (PI-3K)
Das et al., J Cell Physiol 2013 (MAP Kinase Signaling System) : TGFß induced PI 3 kinase dependent Mnk-1 activation is necessary for Ser-209 phosphorylation of eIF4E and mesangial cell hypertrophy ... Moreover, we conclude that TGFß induced noncanonical signaling circuit involving PI 3 kinase dependent Mnk-1 mediated phosphorylation of eIF4E at Ser-209 is required to facilitate mesangial cell hypertrophy