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EGF — PI3

Text-mined interactions from Literome

Venkateswarlu et al., J Cell Sci 1999 : EGF-and NGF stimulated translocation of cytohesin-1 to the plasma membrane of PC12 cells requires PI 3-kinase activation and a functional cytohesin-1 PH domain
Tiganis et al., J Biol Chem 1999 : We have found that TC45 and the TC45-D182A mutant, which is capable of forming stable complexes with TC45 substrates, inhibit almost completely the EGF dependent activation of PI 3-kinase and PKB/Akt ... Thus, TC45 may serve as a negative regulator of growth factor or integrin induced, EGF receptor mediated PI 3-kinase signaling
Fabregat et al., Hepatology 2000 : EGF also activates phosphoinositide 3-kinase ( PI 3-kinase ) and protein kinase B ( PKB/AKT ) in these cells ... We conclude that PI 3-kinase mediates the survival effect of EGF on TGF-beta induced death by acting upstream from the mitochondrial changes, i.e., preventing bcl-x ( L ) down-regulation, cytochrome c release, and activation of caspase-3
Wu et al., Oncogene 2000 (Brain Neoplasms...) : Overexpression of the SIRPalpha1 cDNA diminished EGF induced phosphoinositide-3-OH kinase (PI3-K) activation in U87MG cells
Bilderback et al., J Neurochem 2001 : Finally, this interaction was specific for NGF since EGF did not induce an association of PI 3-kinase with acid SMase
Ellerbroek et al., Cancer Res 2001 (MAP Kinase Signaling System...) : In this study, we compare the roles of EGF induced phosphatidylinositol 3-kinase (PI3K) and mitogen activated protein kinase ( MAPK ) activities in regulation of cellular responses associated with ovarian tumor cell metastasis
Liu et al., Br J Cancer 2001 (Uterine Cervical Neoplasms) : EGF did not stimulate PI-3K/Akt , MEK/MAPK, or p38 MAPK activity in SiHa cells but did transiently activate the c-Jun NH2-terminal kinase (JNK)
Scheving et al., Biochem Biophys Res Commun 2002 : Pharmacologic inhibition of the EGFR kinase abolished the proliferative actions of HGF and EGF, but not insulin, whereas PI-3 kinase inhibition blocked both EGF and insulin actions
Ugi et al., J Biol Chem 2002 : In support of this, we found that the PI 3-kinase inhibitors, wortmannin and LY294002, blocked insulin stimulated but not EGF- or PDGF stimulated Shc phosphorylation
Millar et al., Can J Physiol Pharmacol 2002 : We conclude that the effect of EGF on jejunal glucose transport is mediated at least in part by PKC and PI 3-kinase
Elad-Sfadia et al., J Biol Chem 2002 : Conversely, Ras and galectin-1 co-transfection inhibited the EGF stimulated increase in phosphoinositide 3-kinase (PI3K) activity
Roberts et al., Br J Pharmacol 2003 : 2 alpha ( 2 ) Adrenoceptor mediated vasoconstriction and ERK2 activation in the porcine palmar lateral vein was inhibited in the presence of either the PI 3-kinase inhibitor LY294002, or the EGF receptor tyrosine kinase inhibitor AG1478 suggesting the involvement of both PI 3-kinase and EGF receptor transactivation
Kong et al., Mol Endocrinol 2003 : Overexpression of the PH domain of Gab2 did not affect EGF induced Gab2 phosphorylation, PI3K activation, and DNA synthesis
She et al., Oncogene 2003 (Cell Transformation, Neoplastic) : Furthermore, this compound, but not resveratrol, markedly inhibited EGF induced phosphatidylinositol-3 kinase (PI-3K) and Akt activation
Thoresen et al., Cell Physiol Biochem 2003 : Role of ERK, p38 and PI3-kinase in EGF receptor mediated mitogenic signalling in cultured rat hepatocytes : requirement for sustained ERK activation
Li et al., Gastroenterology 2004 : In intestinal Na absorptive cells, phosphatidylinositol 3-kinase (PI 3-K) is involved in rapid epidermal growth factor (EGF) stimulation of Na absorption by the brush border membrane ( BBM ) Na ( + ) /H ( + ) exchanger NHE3
Maeda et al., Transplant Proc 2004 (Cadaver) : Our results suggest that PI3-kinase/Akt activation by insulin or EGF is beneficial for islet beta cell protection
Deb et al., J Biol Chem 2004 : Pharmacological inhibitors of calmodulin kinase kinase and calmodulin kinases II and III do not inhibit EGF induced Akt activation, and calmodulin antagonist W-7 does not inhibit phosphotyrosine associated PI-3 kinase activation
Perez et al., Eur J Neurosci 2005 : In addition, PACAP and forskolin inhibited basal Akt phosphorylation, and basal and epidermal growth factor (EGF) stimulated phosphatidylinositol 3-kinase (PI 3-K) activities
Mahimainathan et al., American journal of physiology. Renal physiology 2005 : EGF increased PI3-kinase activity resulting in stimulation of PDK-1 and Akt kinase activities ... These data indicate that EGF increases the DNA synthesis in a PI3-kinase dependent but Akt independent manner ... Because EGF activates PI3-kinase , which also regulates DNA synthesis, the effect of PI3-kinase on MAPK activity was also examined
Itakura et al., J Neurochem 2005 : EGF activated both mitogen activated protein kinase ( MAPK ) and phosphatidylinositol 3-kinase ( PI3-kinase ) pathways, and the EGF dependent enhancement of DA release was suppressed by a MAPK kinase inhibitor as well as by PI3-kinase inhibitors ... These results indicate that PI3-kinase participates in the enhancement of neurotransmitter release by two distinct mechanisms : EGF and NGF activate PI3-kinase in the plasma membrane, whereas IGF-1 activates PI3-kinase possibly in the intracellular membrane, leading to enhancement of neurotransmitter release in a MAPK dependent and -independent manner respectively
Ma et al., Mol Cell Biol 2005 : Pharmacological experiments indicate that the EGF induced activation of PKD2 occurs independently of store depletion but requires the activity of phospholipase C (PLC) and phosphoinositide 3-kinase (PI3K)
Nomura et al., Phytochemistry 2005 (Cell Transformation, Neoplastic) : On the other hand, compounds 3 and 4 suppressed EGF induced phosphatidylinositol 3-kinase (PI3K) activation
Galbaugh et al., BMC cell biology 2006 : Treatment of cells with Rapamycin, an inhibitor of mTOR, blocked the effects of EGF on beta-casein promotor driven luciferase activity as effectively as PI-3-kinase inhibitors ... 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
Ichimatsu et al., Mol Carcinog 2007 (Cell Transformation, Neoplastic) : In addition, myricetin, quercetagetin, EGCG, and theaflavins directly inhibited EGF induced phosphatidylinositol 3-kinase (PI3K) activation
El-Sibai et al., J Cell Sci 2007 (Carcinoma) : Upstream of Arp2/3, Cdc42 knockdown inhibited EGF stimulated activation of PI 3-kinase at early ( within 1 minute ) but not late ( within 3 minutes ) time points
Koyama et al., Dev Growth Differ 2008 : Immunoblotting showed that EGF strongly stimulated phosphorylation of extracellular signal regulated kinase-1/2 ( ERK-1/2 ) and weakly stimulated phosphorylation of phospholipase Cgamma1 ( PLCgamma1 ) and phosphatidylinositol-3 kinase (PI3K) in cultured E14 SMG
Scharl et al., Am J Physiol Gastrointest Liver Physiol 2010 : The Crohn 's disease candidate gene, protein tyrosine phosphatase nonreceptor type 2 ( PTPN2 ), has been shown to regulate epidermal growth factor (EGF) induced phosphatidylinositol 3-kinase (PI3K) activation in fibroblasts
Hwang et al., Mol Nutr Food Res 2011 (Fibrosarcoma...) : Capsaicin suppressed EGF induced c-Jun and c-Fos nuclear translocation, and also abrogated the EGF induced phosphorylation of EGF receptor (EGFR), focal adhesion kinase ( FAK ), protein kinase C ( PKC ), phosphatidylinositol 3-Kinase (PI3K)/Akt , extracellular regulated kinase (ERK)1/2, and JNK1/2, an upstream modulator of AP-1
Saxena et al., Antioxid Redox Signal 2013 (Colonic Neoplasms...) : Inhibition of AR also prevented the epidermal growth factor induced phosphorylation of phosphatidylinositol 3-kinase (PI3K) , serine/threonine kinase ( AKT ), c-Jun, c-Fos, PTEN, and FOXO3a, and deoxyribonucleic acid ( DNA ) -binding activity of AP-1
Wu et al., Mol Med Report 2013 : Pretreatment with LY294002 [ a phosphatidylinositol 3-kinase (PI3K) inhibitor ], EGF ( an EGFR agonist ) and AG1478 ( an EGFR inhibitor ) partially reversed IS-induced decreases in cell viability
Pomerance et al., J Neurosci Res 1995 : In astroglial cells cultured in serum-free medium, IGF1, PDGF, and EGF , which stimulate cell proliferation, increased PI(3)-kinase activity immunoprecipitated with anti-phosphotyrosine antibodies as shown by thin layer chromatography and high performance liquid chromatography
Kido et al., Biochem Biophys Res Commun 1995 : We investigated epidermal growth factor (EGF) induced activation of 85-kDa/110-kDa phosphatidylinositol (PI)-3-kinase and 70-kDa S6 kinase in Chinese hamster ovary cells expressing the human EGF receptor
Schuh et al., Mol Biol Cell 1994 : In addition, the ability of EGF to stimulate PI 3-kinase activity and mitogen activated protein kinase activity was enhanced in cells expressing the P1003G EGF receptor
Wiese et al., J Biol Chem 1995 : PDGF and insulin, but not EGF , caused a transient increase in the amount PI 3'-K activity coprecipitated with tyrosine phosphorylated proteins
Newberry et al., Biochem Biophys Res Commun 1995 (Carcinoma, Squamous Cell) : EGF stimulated PI 3-kinase activity was also reduced by approximately 60 % during S phase as compared to G1 phase
Soltoff et al., J Biol Chem 1996 : Although epidermal growth factor (EGF) activates phosphoinositide (PI) 3-kinase activity in a number of types of cells or cell lines, in most cases that we have investigated the p85 regulatory subunit of PI 3-kinase does not appear to bind directly to the EGF receptor ... Previously we demonstrated that EGF dependent activation of PI 3-kinase activity in A431 cells is accompanied by the binding of p85 to ErbB3, an EGF receptor homologue ... p120cbl was also present in A431 cells and offers an additional pathway by which EGF can activate PI 3-kinase in these cells
Khurana et al., J Biol Chem 1996 : In rabbit ileum studied with the Ussing chamber-voltage clamp technique, EGF stimulation of active NaCl absorption is inhibited by the selective PI 3-kinase inhibitor wortmannin
Kole et al., J Biol Chem 1996 : However, stearyl 3S-peptide-I had no effect on the EGF stimulated activation of PI-3-kinase and mitogen activated protein kinase in CHO/EGF-R cells
Huang et al., Mol Cell Biol 1996 (Cell Transformation, Neoplastic) : ( i ) EGF not only induced a high level of PI 3-kinase activity by itself but also enhanced insulin induced PI 3-kinase activity in JB6 P+ cells, the EGF induced PI-3 kinase activity could be blocked by constitutive overexpression of a dominant negative P85 subunit of PI 3-kinase ( deltaP85 ), and insulin could markedly promote EGF induced AP-1 activity in a dose dependent manner in JB6 P+ cells as well as promote EGF induced JB6 P+ cell transformation
Uribe et al., J Biol Chem 1996 : Furthermore, only EGF increased PI 3-kinase activity in an in vitro kinase assay ... Our data suggest that EGF activates PI 3-kinase and that its lipid products may mediate the inhibitory effect of EGF on calcium dependent chloride secretion
Gnudi et al., Mol Endocrinol 1997 : Similarly, insulin and epidermal growth factor activation of total ( no immunoprecipitation ) PI3-kinase activity in both cytosol and total cellular membranes and insulin stimulation of glucose transport were not affected by expression of dominant negative ras
Krymskaya et al., Am J Physiol 1997 : In this study, we postulated that TGF-beta 1 may modulate EGF induced PI 3-kinase activation ... In cultured hASM cells, EGF induced a 5.7 +/- 1.2-fold activation of PI 3-kinase compared with diluent treated cells ... Although TGF-beta 1 alone did not alter PI 3-kinase activation, TGF-beta 1 markedly enhanced EGF induced PI 3-kinase activity, with a 16.6 +/- 1.9-fold increase over control cells treated with diluent alone ... EGF significantly increased the association of PI 3-kinase with tyrosine phosphorylated proteins, and TGF-beta 1 pretreatment before EGF stimulation apparently did not alter this association
van Weering et al., Mol Cell Biol 1998 : Here we show that several growth factors ( basic fibroblast growth factor [bFGF ], platelet derived growth factor [ PDGF ], and epidermal growth factor [EGF ; to activate an EGF receptor-Ret chimeric receptor ] ) all activate PI 3-kinase in vivo in the neuroectoderm derived cell line SKF5
Boelsma et al., Acta Derm Venereol 1998 (Dermatitis, Allergic Contact) : SKALP expression was induced by serum, epidermal growth factor and fibroblasts
Zhang et al., Curr Eye Res 1998 : Incubation of the cells with wortmannin, a PI 3-kinase inhibitor, abolished the EGF stimulated PI 3-kinase activity, but potentiated the EGF stimulated PLD activity
Lipson et al., J Pharmacol Exp Ther 1998 : A synthetic EGF receptor kinase inhibitor showed selective inhibitor properties when tested for EGF induced receptor autophosphorylation, MAPK activation, PI3K activation, entry into S phase and cyclin E-associated kinase activity
Bolander et al., Am J Physiol 1998 : In contrast, the effect on EGF receptors is mediated by tyrosine phosphorylation and phosphatidylinositol 3-kinase (PI3K) , since it can be blocked by either a tyrosine kinase inhibitor or by a PI3K inhibitor
Takahashi et al., J Cell Physiol 1999 : IGF-I induced PI 3-kinase activation is generally mediated via insulin receptor substrate (IRS)-1, but EGF induced PI 3-kinase activation is mediated by various signalling molecules such as ErbB3 and c-Cbl in different cells