PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28535513-1 2017 BACKGROUND: Protein Kinase C-alpha (PKC-alpha) and epidermal growth factor receptor (EGFR) are both involved in diabetic kidney disease; however, the connection between these two proteins during high glucose-induced podocyte injury remains uncertain. Glucose 200-207 epidermal growth factor receptor Rattus norvegicus 85-89 28535513-8 2017 Consistently, in vitro high glucose treated podocytes, membranous EGFR is downregulated with increased PKC-alpha. Glucose 28-35 epidermal growth factor receptor Rattus norvegicus 66-70 23423570-5 2013 Using cultured human keratinocytes and a diabetic rat model, the current study shows that a high-glucose environment enhanced IL-8 production via epidermal growth factor receptor (EGFR)-extracellular signal-regulated kinase (ERK) pathway in a reactive oxygen species (ROS)-dependent manner in keratinocytes. Glucose 97-104 epidermal growth factor receptor Rattus norvegicus 180-184 26527065-7 2016 Also via EGFR, CRAMP stimulates glucose-stimulated insulin secretion ex vivo by rat islets. Glucose 32-39 epidermal growth factor receptor Rattus norvegicus 9-13 26175156-12 2015 Finally, inhibitors of epidermal growth factor receptor (EGFR) and downstream PI3K/Akt, or ADAM17 itself, prevented high glucose-induced HIF-1alpha activation and ADAM17 up-regulation. Glucose 121-128 epidermal growth factor receptor Rattus norvegicus 23-55 26175156-12 2015 Finally, inhibitors of epidermal growth factor receptor (EGFR) and downstream PI3K/Akt, or ADAM17 itself, prevented high glucose-induced HIF-1alpha activation and ADAM17 up-regulation. Glucose 121-128 epidermal growth factor receptor Rattus norvegicus 57-61 25758431-8 2015 In vitro, either pharmacological inhibition of EGFR/AKT or sh-RNA silencing of EGFR significantly inhibited high concentration glucose (HG)-induced ROS generation and subsequently cell apoptosis in both cardiac H9C2 cells and primary rat cardiomyocytes, respectively. Glucose 127-134 epidermal growth factor receptor Rattus norvegicus 47-51 25758431-8 2015 In vitro, either pharmacological inhibition of EGFR/AKT or sh-RNA silencing of EGFR significantly inhibited high concentration glucose (HG)-induced ROS generation and subsequently cell apoptosis in both cardiac H9C2 cells and primary rat cardiomyocytes, respectively. Glucose 127-134 epidermal growth factor receptor Rattus norvegicus 79-83 23423570-5 2013 Using cultured human keratinocytes and a diabetic rat model, the current study shows that a high-glucose environment enhanced IL-8 production via epidermal growth factor receptor (EGFR)-extracellular signal-regulated kinase (ERK) pathway in a reactive oxygen species (ROS)-dependent manner in keratinocytes. Glucose 97-104 epidermal growth factor receptor Rattus norvegicus 146-178 19605547-0 2009 EGFR-PLCgamma1 signaling mediates high glucose-induced PKCbeta1-Akt activation and collagen I upregulation in mesangial cells. Glucose 39-46 epidermal growth factor receptor Rattus norvegicus 0-4 21806601-6 2012 In VSMCs grown in conditions of high glucose (25 mM), an Src-dependent elevation in EGF receptor phosphorylation was observed. Glucose 37-44 epidermal growth factor receptor Rattus norvegicus 84-96 21806601-7 2012 Ang-(1-7) inhibited both Ang II- and glucose-induced transactivation of EGF receptor. Glucose 37-44 epidermal growth factor receptor Rattus norvegicus 72-84 21806601-8 2012 The inhibition of high glucose-mediated Src-dependant transactivation of EGF receptor by Ang-(1-7) could be prevented by a selective Mas receptor antagonist, D-Pro7-Ang-(1-7). Glucose 23-30 epidermal growth factor receptor Rattus norvegicus 73-85 20836700-1 2011 Betacellulin (BTC), a ligand of the epidermal growth factor receptor, has been shown to promote growth and differentiation of pancreatic beta-cells and to improve glucose metabolism in experimental diabetic rodent models. Glucose 163-170 epidermal growth factor receptor Rattus norvegicus 36-68 19605547-2 2009 We have recently shown that epidermal growth factor receptor (EGFR) transactivation mediates high glucose (HG)-induced collagen I upregulation through PI3K-PKCbeta1-Akt signaling in mesangial cells (MC). Glucose 98-105 epidermal growth factor receptor Rattus norvegicus 28-60 19605547-2 2009 We have recently shown that epidermal growth factor receptor (EGFR) transactivation mediates high glucose (HG)-induced collagen I upregulation through PI3K-PKCbeta1-Akt signaling in mesangial cells (MC). Glucose 98-105 epidermal growth factor receptor Rattus norvegicus 62-66 17622510-0 2007 Collagen I induction by high glucose levels is mediated by epidermal growth factor receptor and phosphoinositide 3-kinase/Akt signalling in mesangial cells. Glucose 29-36 epidermal growth factor receptor Rattus norvegicus 59-91 19211711-2 2009 The serine/threonine kinase Akt mediates glucose-induced upregulation of collagen I in mesangial cells through transactivation of the EGF receptor (EGFR). Glucose 41-48 epidermal growth factor receptor Rattus norvegicus 134-146 19211711-2 2009 The serine/threonine kinase Akt mediates glucose-induced upregulation of collagen I in mesangial cells through transactivation of the EGF receptor (EGFR). Glucose 41-48 epidermal growth factor receptor Rattus norvegicus 148-152 19211711-7 2009 Finally, pharmacologic and dominant negative inhibition of EGFR blocked glucose-induced activation of PKC-beta1, phosphorylation of AktS473, activation of AP-1, and upregulation of TGF-beta1. Glucose 72-79 epidermal growth factor receptor Rattus norvegicus 59-63 17622510-14 2007 Since signalling through the epidermal growth factor receptor (EGFR) can activate PI3K-Akt, we studied its activation by high glucose levels. Glucose 126-133 epidermal growth factor receptor Rattus norvegicus 29-61 17622510-14 2007 Since signalling through the epidermal growth factor receptor (EGFR) can activate PI3K-Akt, we studied its activation by high glucose levels. Glucose 126-133 epidermal growth factor receptor Rattus norvegicus 63-67 17622510-17 2007 Specific EGFR inhibition (AG1478, 5 micromol/l or dominant-negative EGFR) blocked high glucose-induced pAktS473, phosphorylation on threonine 308 and activation of the EGFR downstream target p44 extracellular signal-regulated kinase (Erk) mitogen-activated protein kinase. Glucose 87-94 epidermal growth factor receptor Rattus norvegicus 9-13 17622510-17 2007 Specific EGFR inhibition (AG1478, 5 micromol/l or dominant-negative EGFR) blocked high glucose-induced pAktS473, phosphorylation on threonine 308 and activation of the EGFR downstream target p44 extracellular signal-regulated kinase (Erk) mitogen-activated protein kinase. Glucose 87-94 epidermal growth factor receptor Rattus norvegicus 68-72 17622510-17 2007 Specific EGFR inhibition (AG1478, 5 micromol/l or dominant-negative EGFR) blocked high glucose-induced pAktS473, phosphorylation on threonine 308 and activation of the EGFR downstream target p44 extracellular signal-regulated kinase (Erk) mitogen-activated protein kinase. Glucose 87-94 epidermal growth factor receptor Rattus norvegicus 68-72 17622510-18 2007 Finally, EGFR inhibition also blocked high glucose-induced collagen I upregulation at transcriptional and protein levels. Glucose 43-50 epidermal growth factor receptor Rattus norvegicus 9-13 17622510-19 2007 CONCLUSIONS/INTERPRETATION: We conclude that EGFR-PI3K-Akt signalling mediates high glucose-induced collagen I upregulation in mesangial cells and that this pathway is activated in diabetic glomeruli. Glucose 84-91 epidermal growth factor receptor Rattus norvegicus 45-49 31882563-10 2020 Our findings identify a novel glucose/HB-EGF/EGFR axis implicated in beta-cell compensation to increased metabolic demand. Glucose 30-37 epidermal growth factor receptor Rattus norvegicus 45-49 31882563-3 2020 The aim of this study was to determine the role of the EGFR ligand Heparin-Binding EGF-like Growth Factor (HB-EGF) in the beta-cell proliferative response to glucose, a beta-cell mitogen and key regulator of beta-cell mass in response to increased insulin demand. Glucose 158-165 epidermal growth factor receptor Rattus norvegicus 55-59 31882563-5 2020 In rat islets, inhibition of EGFR or HB-EGF blocks the proliferative response not only to HB-EGF but also to glucose. Glucose 109-116 epidermal growth factor receptor Rattus norvegicus 29-33