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ANGPT2 — EGFR

Pathways - manually collected, often from reviews:

• WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: EFNA1/FGF1/FGF11/FGF10/EFNA2/EGF/FGF12/CSF1/ANGPT4/ANGPT2/ANGPT1/VEGFA/EFNA3/EFNA4/EFNA5/FGF14/FGF19/FGF17/FGF18/FGF2/FGF3/FGF4/FGF6/FGF7/FGF8/FGF9/FIGF/HGF/IGF1/INS/INS/KITLG/VEGFC/VEGFB/PDGFB/PGF/PDGFA/NGF/PDGFC/FGF21/FGF22/PDGFD/FGF20/FGF16 → FGFR2/KDR/INSR/FGFR3/IGF1R/KIT/FGFR1/EPHA2/EGFR/CSF1R/FGFR4/FLT1/FLT4/NGFR/MET/PDGFRA/PDGFRB/TEK (activation)
  

Text-mined interactions from Literome

Moriguchi et al., Circ Res 1999 : Here, we report the involvement of EGF-R in Ang II-induced synthesis of fibronectin and transforming growth factor-beta ( TGF-beta ) in cardiac fibroblasts
Mondorf et al., FEBS Lett 2000 : Here, we studied the role of the epidermal growth factor receptor (EGFR) and platelet derived growth factor receptor ( PDGFR ) in Ang II-induced ERK1/2 activation in human mesangial cells ... Ang II induced activation of ERK1/2 via the AT(1) receptor, and this response was blocked by the PDGFR-selective tyrosine kinase inhibitor AG1295, but not by AG1478, an EGFR-selective tyrosine kinase inhibitor, indicating participation of the PDGFR, but not of the EGFR in Ang II-induced ERK1/2 activation ... In conclusion, our data show that Ang II-induced activation of mitogenic signalling cascade in human mesangial cells involves ligand independent activation of the PDGFR, but not of the coexpressed EGFR
Murasawa et al., J Biol Chem 2000 (Calcium Signaling) : In this study, we tested the involvement of Pyk2 and EGF-R in Ang II-induced activation of JNK and c-Jun in cardiac fibroblasts
Bokemeyer et al., Kidney Int 2000 (Coronary Artery Disease...) : A time dependent tyrosine phosphorylation of the EGFR in response to Ang II was observed that was mediated by the Ang II type 1 receptor ... Furthermore, Ang II induced the binding of the adaptor protein Shc to the EGFR , leading to phosphorylation of Shc
Ushio-Fukai et al., Arterioscler Thromb Vasc Biol 2001 : Ang II induces phosphorylation of the epidermal growth factor (EGF) receptor ( EGF-R ), which serves as a scaffold for various signaling molecules
Shah et al., Mol Endocrinol 2002 : In COS-7 cells transiently expressing the rat AT1A-R, Ang II also caused ERK activation through EGF-R transactivation
Kagiyama et al., Circulation 2002 (Hypertension...) : EGFR-AS , but not EGFR-sense, normalized the LV/BW in Ang II-infused rats ( 2.32+/-0.06 ; P < 0.01 ) and attenuated Ang II-enhanced EGFR expression and ERK phosphorylation ... Ang II requires EGFR to mediate ERK activation in VSMCs and the heart
Lin et al., Prostate 2003 : Because the pressor peptide Ang II signals through GPCRs, we tested the possibility that Ang II could transactivate ErbB1/ErbB2 in human prostate stromal ( hPS ) cells ... Furthermore, Ang II was able to transactivate both ErbB1 and ErbB2, and this transactivation activity could be abolished by pretreatment with [ Glu-52 ] -diphtheria toxin/CRM197, a specific inhibitor of HB-EGF bioactivity
Andresen et al., Hypertension 2003 (MAP Kinase Signaling System) : To examine the role of the EGFR in Ang II-mediated phosphorylation of ERK we utilized 100 nmol/L wortmannin to inhibit EGFR signaling to ERK and T19N RhoA to block Ang II-mediated ERK phosphorylation
Nose et al., Hypertens Res 2003 (MAP Kinase Signaling System) : Our objective in the present study was to assess the effect of Ang II on glucose transporter 1 (GLUT1) gene expression and to clarify the involvement of EGF-R in Ang II-mediated GLUT1 mRNA expression in glomerular mesangial cells
Li et al., J Pharmacol Exp Ther 2005 : In addition, the inhibitor of arachidonic acid ( AA ) metabolism 5,8,11,14-eicosatetraynoic acid ( ETYA ) reduced both Ang II- and AA-induced EGFR transactivation
Yang et al., Mol Cells 2005 (MAP Kinase Signaling System) : Furthermore Ang II-stimulated proliferation and migration of smooth muscle cells were significantly blunted by inhibiting MMPs and EGFR and applying HB-EGF neutralization antibody, indicating that MMPs, HB-EGF and EGFR activation is necessary for Ang-II stimulated migration and proliferation of smooth muscle cells
Shah et al., Trends Pharmacol Sci 2006 (Kidney Diseases) : Ang II causes renal lesions through the activation of tumor necrosis factor (TNF)-alpha converting enzyme ( TACE, also called a disintegrin and a metalloproteinase domain 17 ) and the release of transforming growth factor (TGF)-alpha, which binds to and activates the epidermal growth factor receptor
Chen et al., J Am Soc Nephrol 2006 (Hypertrophy...) : Ang II elicited release of soluble heparin binding EGF-like growth factor ( HB-EGF ) from AT1R/Cl4 cells, and Ang II-induced EGFR activation was prevented by pretreatment with the specific HB-EGF inhibitor CRM197 or the metalloproteinase inhibitors batimastat or phenanthroline, none of which had any effect on EGFR activation by exogenously administered EGF
Niu et al., Cancer Res 2007 (Breast Neoplasms...) : Human epidermal growth factor receptor 2 regulates angiopoietin-2 expression in breast cancer via AKT and mitogen activated protein kinase pathways
Pham et al., J Cell Physiol 2008 : The p38 ( MAPK ) selective inhibitor, SB202190, but not the MEK selective inhibitor, PD98059, or the EGFR kinase inhibitor, AG1478, inhibited Ang II-dependent COX-2 expression and CREB phosphorylation
Olson et al., Hypertension 2008 : We also found that Ang II does not transactivate the epidermal growth factor receptor in adult cardiac fibroblasts, because pretreatment with 1 mumol/L of AG 1478 did not significantly inhibit [ ( 3 ) H ] -thymidine incorporation or ERK 1/2 activation ... Collectively, these data demonstrate that Ang II does not transactivate the epidermal growth factor receptor in adult rat cardiac fibroblasts to activate ERK 1/2, a common pathway described in vascular smooth muscle and other cell types, but rather occurs via activation of distinct parallel signaling pathways mechanistically controlled by intracellular Ca ( 2+ ) and PKCdelta
Nakai et al., J Dermatol Sci 2008 : Although Ang II did not activate the EGFR , the expression levels of EGFR protein were increased in HaCaT cells treated with Ang II ( 1 microM ) at 6h ... These results suggest that Ang II enhances the cell proliferation and EGFR expression via superoxide production under the regulation of NO in HaCaT cells, implying that Ang II may regulate the proliferation, differentiation and tumorigenesis of the epidermis by harmonizing the superoxide and NO production
Freeman et al., Arch Biochem Biophys 2010 : In this study, Ang II increased phosphorylation of the EGFR and MAPK in cultured VSMC and these effects were attenuated by the cPLA(2) inhibitor arachidonyl trifluoromethyl ketone ( AACOCF ( 3 ) ), and restored by addition of ArAc
Shimizu et al., Life Sci 2012 (Arteriosclerosis) : The effect of indoxyl sulfate and Ang II on phosphorylation of ERK and epidermal growth factor receptor (EGFR) , and migration were determined using VSMCs
Eguchi et al., J Biol Chem 1998 : In the present study, we found Ang II rapidly induced the tyrosine phosphorylation of the epidermal growth factor (EGF) receptor and its association with Shc and Grb2
Murasawa et al., Circ Res 1998 : Ang II induced a rapid tyrosine phosphorylation of EGF-R in association with phosphorylation of Shc protein and ERK activation ... Our results demonstrated that in cardiac fibroblasts Ang II-induced ERK activation and its mitogenic signals are dominantly mediated by EGF-R transactivated in a Ca2+/calmodulin dependent manner and suggested that the effects of Ang II on cardiac fibroblasts should be interpreted in association with the signaling pathways regulating cellular proliferation and/or differentiation by growth factors
Eguchi et al., Hypertension 1999 : Although a selective EGFR kinase inhibitor completely abolished Ang II-induced recruitment of Grb2 to EGFR and markedly attenuated Ang II-induced ERK activation, it had no effect on Ang II-induced PYK2 tyrosine phosphorylation or its association with c-Src and Grb2