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PI3 — RAF1

Text-mined interactions from Literome

Sun et al., Curr Biol 2000 : Pharmacological inhibitors of PI 3-kinase also blocked both activation and Ser338 phosphorylation of Raf-1 induced by epidermal growth factor (EGF)
Krepinsky et al., Cell Signal 2005 : Although phosphatidylinositol-3-kinase (PI3-K) may mediate Raf-1 activation, PI3-K inhibition with wortmannin or LY294002 had no effect on stretch induced Raf-1 activation
Romano et al., Endocrinology 2006 : Under the same conditions, PI3K and Akt inhibition also both increased Raf-1 kinase activity and the levels of GTP bound ( active form ) monomeric G protein Rap1, which suggests that a down-regulation of the ERK-1/2 cascade is induced by the PI3K/Akt signaling pathway in unstimulated cells
Banerjee et al., Endocrinology 2009 : This study shows that in the human endometrial cell line, HES, CG, acting via its G-protein coupled receptor, phosphorylates protein kinase B, c-Raf , and ERK1/2 in a phosphatidylinositol 3-kinase (PI3K) dependent manner
Chang et al., Pharmacol Res 2009 : YC-1 mediated Raf-1 activation was inhibited by an sGC inhibitor ( ODQ ), a PKG inhibitor ( KT-5823 ), a Ras inhibitor ( manumycin A ), a dominant negative Ras mutant ( RasN17 ), a protein kinase C-alpha (PKC-alpha) inhibitor ( Ro 32-0432 ), and a phosphoinositide-3-OH-kinase (PI3K) inhibitor ( LY 294002 )
King et al., Mol Cell Biol 1997 : We conclude that integrin mediated adhesion to fibronectin results in the accumulation of the PI 3-kinase products PI ( 3,4 ) P2 and PI ( 3,4,5 ) P3 as well as the PI 3-kinase dependent activation of the kinases Raf-1 , Mek-1, Erk-2, and AKT and that PI 3-kinase may function upstream of Raf-1 but downstream of Ras in integrin activation of Erk-2 MAP and AKT kinases