◀ Back to GRAP2

EGF — GRAP2

Text-mined interactions from Literome

McCawley et al., Mol Pharmacol 2000 (MAP Kinase Signaling System) : However, forskolin effectively inhibited EGF dependent activation of c-Jun N-terminal kinase and p38 , demonstrating that cAMP selectively interferes with a different subset of growth factor induced mitogen activated protein kinase signaling cascades than reported previously in fibroblasts
Yang et al., J Membr Biol 2001 : Taken together, EGF stimulates Erk1/2 ; p38 and cPLA2 activity
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
Raucci et al., J Biol Chem 2004 : FGF- and NGF induced growth inhibition is accompanied by a strong and sustained activation of ERK1/2 and p38 MAPK and a decrease of AKT phosphorylation, whereas EGF induces a much more transient activation of p38 and ERK1/2 and increases AKT phosphorylation
Raspaglio et al., Oncol Res 2003 (Carcinoma, Squamous Cell...) : Mitogen activated protein kinase ( MAPK ) analysis revealed that in Hep2 cells, but not in CO-K3 cells, EGF induced a time dependent phosphorylation of p42, p44, p38 , and p46
Tong et al., Cell Signal 2004 : EGF stimulated comparable or lower Erk1/2, p38 and Akt phosphorylation while IL-1beta induced p38 phosphorylation in the fibroblast cell lines
Frey et al., J Biol Chem 2004 : Activation of p38 in intestinal epithelial cells through EGF receptor was abolished by blockade of Src family tyrosine kinase signaling but not inhibition of phosphatidylinositol 3-kinase or protein kinase C. Taken together, these data suggest that Src family kinase dependent p38 activation is a key component of a signaling switch routing EGF stimulated responses to epithelial cell migration/restitution rather than proliferation during wound closure
Sugaru et al., American journal of physiology. Renal physiology 2005 (Glomerulonephritis) : SMP-534 inhibited TGF-beta induced p38 mitogen activated protein kinase ( p38 ) activation but did not inhibit epidermal growth factor (EGF) induced extracellular signal related kinase ( ERK ) activation
Harrington et al., Obesity (Silver Spring) 2007 : Selective inhibition of the EGF receptor (EGFR) with AG1478 blocked ERK and p38 activation at both concentrations ; however, selective inhibition of the ErbB2 receptor (EB2R) with AG825 or small interfering RNA ( siRNA ) blocked low but not high EGF activation of ERK and p38
Ostrander et al., Cancer Res 2007 (Breast Neoplasms) : Knockdown of Brk by stable expression of short hairpin RNA ( shRNA ) in T47D breast cancer cells decreases proliferation and blocks epidermal growth factor (EGF)- and heregulin induced activation of Rac GTPase, extracellular signal regulated kinase ( ERK ) 5, and p38 mitogen activated protein kinase ( MAPK ) but not Akt, ERK1/2, or c-Jun NH ( 2 ) -terminal kinase
He et al., Mol Carcinog 2008 (Cell Transformation, Neoplastic) : The K ( d ) value for EGCG binding to the Fyn SH2 domain was 0.367 +/- 0.122 microM and B ( max ) was 1.35 +/- 0.128 nmol/mg. Compared with control JB6 Cl41 cells, EGF induced phosphorylation of p38 MAP kinase (p38 MAPK) ( Thr180/Tyr182 ), ATF-2 ( Thr71 ) and signal transducer and activator of transcription 1 ( STAT1 ) ( Thr727 ) was decreased in siRNA-Fyn-JB6 cells
Park et al., Cell Prolif 2008 (Calcium Signaling) : EGF induced phosphorylation of p38 and p44/42 MAPKs, and this was blocked by SB 203580 ( a p38 MAPK inhibitor ) and PD 98059 ( a p44/42 MAPK inhibitor ), respectively
Baek et al., Oncol Rep 2008 (Carcinoma...) : In addition, EGF induced the activation of extracellular signal regulated kinase-1/2 ( ERK-1/2 ) and P38 mitogen activated protein kinase ( MAPK ) but not the activation of c-Jun amino terminal kinase
Song et al., Cancer Lett 2009 : EGF treatment induced a near-immediate increase in p38 MAPK phosphorylation together with inactivation of ERK1/2
Xu et al., Mol Cell 2010 (MAP Kinase Signaling System) : Conversely, depletion of p38alpha MAP kinase activity suppresses EGF receptor signaling and downstream Erk MAP kinase signaling, as well as autocrine EGF receptor dependent proliferation
Sabri et al., Cell Biochem Funct 2011 (MAP Kinase Signaling System) : In this study, we investigated the effects of PI3K/AKT, ERK1/2, P38 and JNK on EGF signalling in hMSCs