Gene interactions and pathways from curated databases and text-mining

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EGFR — PIK3R1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Ram et al., J Cell Physiol 2000 (Breast Neoplasms) : Furthermore, erbB-3 principally mediated the direct recruitment of p85 in cells stimulated by HRG or EGF, indicating that, in addition to the high-level activation of PI3K by p185(erbB-2) / erbB-3, EGFR/erbB-3 heterodimer interaction is essential for the weak but significant level of PI3K activated by EGF in cells that express normal EGFR levels
Wu et al., Oncogene 2000 (Brain Neoplasms...) : These data reveal a pathway that negatively regulates EGFR induced PI3-K activation in glioblastoma cells and involves interactions between SHP2 and tyrosine phosphorylated SIRPalpha1
von Lindern et al., Oncogene 2001 (Cell Transformation, Neoplastic...) : However, while v-ErbB transformed cells and normal progenitors depended on PI3K signaling for renewal, c-ErbB also induces progenitor expansion by PI3K independent mechanisms
Viñals et al., Mol Cell Biol 2001 : We established that TGF-beta1 stimulated the expression of TGF-alpha mRNA and protein, the tyrosine phosphorylation of a 170-kDa membrane protein representing the epidermal growth factor (EGF) receptor , and the delayed activation of PI3K/Akt and p42/p44 MAPK
Thomas et al., J Biol Chem 2002 (Calcium Signaling) : Together, these data indicate that H ( 2 ) O ( 2 ) promotes calcium dependent eNOS activity through a coordinated change in the phosphorylation status of the enzyme mediated by Src- and ErbB receptor dependent PI 3-K activation
Chakravarti et al., Cancer Res 2002 (Brain Neoplasms...) : It was found that BCNU inhibited radiation induced apoptosis through EGFR mediated activation of PI3-K/AKT via RAS
Arboleda et al., Cancer Res 2003 (Breast Neoplasms...) : Furthermore, expression of kinase dead AKT2 ( 181 amino acid methionine [ M ] ), and not kinase dead AKT1 ( 179M ) or AKT3 ( 177M ), was capable of blocking invasion induced by either human epidermal growth factor receptor-2 ( HER-2 ) overexpression or by activation of PI3-K
Zhuang et al., American journal of physiology. Renal physiology 2004 : These results show that EGFR activation is required for RPTC proliferation and migration and that proliferation is mediated by PI3K , whereas migration is mediated by p38
Nicholl et al., J Vasc Surg 2005 : uPA activation of PI3K and MKK3/6 was EGFR dependent and that of MEK1 was EGFR independent
Shah et al., J Cell Physiol 2006 (MAP Kinase Signaling System) : However, the extent to which EGF-R transactivation is essential for GPCR agonist stimulated PI3K activation is not known ... In C9 hepatocytes, agonist activation of AT1 angiotensin II ( AT1-R ), lysophosphatidic acid (LPA), and EGF receptors caused phosphorylation of Akt through activation of the EGF-R in a PI3K dependent manner
Ihle et al., Mol Cancer Ther 2005 (Carcinoma, Non-Small-Cell Lung...) : Recent work shows that phosphatidylinositol-3-kinase (PI3-K) is coupled to the EGFR only in NSCLC cell lines expressing ErbB-3 and that EGFR inhibitors do not inhibit PI3-K signaling in these cells
Zhang et al., J Biol Chem 2006 : In this study we investigated a potential link between the PI3K-Akt pathway and the cigarette smoke ( CS ) -stimulated epidermal growth factor receptor mediated FRA-1 induction in non-oncogenic HBE cells
Zhan et al., Cancer Res 2006 (Breast Neoplasms...) : The ability of heterodimers to induce invasion required the ErbB1 kinase activity and required activation of PI3K , Ras/mitogen activated protein kinase, and phospholipase Cgamma1 signaling pathways
Kolb et al., Int J Cancer 2007 (Pancreatic Neoplasms) : HRGs induced phosphorylation of different ErbB receptors as well as activation of MAPK, p38MAPK, JNK and PI3K in a cell- and ligand-specific manner
Tétreault et al., J Cell Physiol 2008 : Epidermal growth factor receptor dependent PI3K-activation promotes restitution of wounded human gastric epithelial monolayers ... In conclusion, the present results indicate that EGFR dependent PI3K activation promotes restitution of wounded human gastric epithelial monolayers
Nie et al., Mech Dev 2007 : PI3K and Erk MAPK mediate ErbB signaling in Xenopus gastrulation
Liu et al., Pathophysiology : the official journal of the International Society for Pathophysiology / ISP 2007 : Work with genetic manipulations, as well as pharmacological agents with cell culture models, have demonstrated that the cardiotonic steroid stimulated endocytosis of the plasmalemmal Na/K-ATPase requires caveolin and clathrin as well as the activation of c-Src, transactivation of the EGFR and activation of PI3K
Raufman et al., J Cell Physiol 2008 (Colonic Neoplasms) : Deoxycholyltaurine rescues human colon cancer cells from apoptosis by activating EGFR dependent PI3K/Akt signaling
Lin et al., Toxicol Appl Pharmacol 2008 : LPS stimulated Src, PYK2, EGFR , and Akt phosphorylation and VCAM-1 expression were attenuated by the inhibitors of Src ( PP1 ), EGFR ( AG1478 ), PI3-K ( LY294002 and wortmannin ), and Akt ( SH-5 ), respectively, or transfection with siRNAs of Src or Akt and shRNA of p110
Cao et al., Cell Signal 2008 : Inhibition of EGFR also suppresses UV-induced activation of PI3K/AKT/mTOR/S6K and NF-kappaB signal transduction pathways
Tabassam et al., Cell Microbiol 2009 : Pharmacologic inhibitors of PI3K or mitogen activated protein kinase kinase ( MEK ), Akt knock-down and EGFR knock-down showed that H. pylori infection induced the activation of EGFR -- > PI3K -- > PI3K dependent kinase 1 -- > Akt -- > extracellular signal regulated kinase signalling pathways, the inactivation of glycogen synthase kinase 3beta and interleukin-8 production
Nagy et al., J Infect Dis 2009 : H. pylori enhanced PI3K-AKT signaling in a Src- and epidermal growth factor receptor dependent manner, which was also mediated by a functional cag secretion system and peptidoglycan
Wheeler et al., Cancer Biol Ther 2009 (Carcinoma, Non-Small-Cell Lung...) : We now present data that Src family kinases (SFKs) are highly activated in cetuximab-resistant cells and enhance EGFR activation of HER3 and PI(3)K/Akt
Yin et al., Invest Ophthalmol Vis Sci 2010 : LL-37 enhanced the closure of a scratch wound in cultured HCECs and partially rescued HG-attenuated wound healing in an EGFR- and a PI3K dependent manner and restored HG-impaired EGFR signaling in cultured porcine corneas
Bai et al., Life Sci 2010 (Carcinoma, Hepatocellular...) : The phosphorylation of EGFR and Akt were elevated in EP1 agonist treated cells, and both EGFR and PI3K inhibitors suppressed the upregulation of survivin induced by PGE ( 2 ) or EP1 agonist
Su et al., Life Sci 2010 (Adenocarcinoma...) : Immunoblot showed that NFD inhibited EGFR phosphorylation and the activation of PI3K/Akt , downstream molecules of EGFR pathway, in A549 cells
Krishnaswamy et al., Endocrinology 2010 : Thus, EGFR may simultaneously activate c-Src and PI3K to amplify the OT signaling to increase the output of PGF ( 2 alpha ) in bEEL cells
Zuo et al., Breast Cancer Res 2010 (Breast Neoplasms...) : To define the potential inter-mediate steps between mPRalpha and PI3K, we demonstrated that mPRalpha, caveolin-1 (Cav-1), and epidermal growth factor receptor (EGFR) are colocalized in the membrane of caveolar vesicle and the P4-repressed EMT in MB468 cells can be blocked by EGFR inhibitor ( AG1478 ) and PI3K inhibitor ( wortmannin )
Wakasaki et al., Neoplasia (New York, N.Y.) 2010 (Carcinoma, Squamous Cell...) : Little is known, however, about a role of CIN85 in EGFR signaling as well as its relevance to tumor development and progression of HNSCC
He et al., Ann Oncol 2012 (Breast Neoplasms...) : Human epidermal growth factor receptor ( HER2 ), insulin receptor and IGF-I receptor involve the same PI3K/AKT/mTOR signaling, and different antidiabetic pharmacotherapy may differentially affect this pathway, leading to different prognoses of HER2+ breast cancer
Meira et al., Molecular cancer 2011 : The combination of PD98059 and matuzumab did not show the same effect suggesting that PI3K is an important effector of EGFR signaling in matuzumab treated cells
Zhao et al., J Lipid Res 2012 : Further studies showed that TNF-a decreased expression of the antiapoptotic proteins Bcl-2 and Bcl-xL, decreased I?Ba and PPAR?, and also inhibited PI3K dependent Akt and EGFR signaling
Tajeddine et al., J Biol Chem 2012 (MAP Kinase Signaling System) : This was associated with a decreased phosphorylation and activation of EGFR and with a subsequent disruption of PI3K/Akt and MAPK downstream pathways
Tsai et al., Toxicon 2012 (MAP Kinase Signaling System...) : These findings suggest that CTX III inhibited the EGF induced invasion and migration of MDA-MB-231 cells via EGFR dependent PI3K/Akt , ERK1/2, and NF-?B signaling, leading to the down-regulation of MMP-9 expression
Tabara et al., PloS one 2012 (Lung Neoplasms) : However, constitutive activation of EGFR downstream signaling, PI3K/Akt , was observed even after loss of the mutated EGFR gene in all resistant cell lines even in the presence of the drug
Schroeder et al., Mol Biol Cell 2012 : In this study we show that EGFR activation leads to a pronounced src mediated tyrosine phosphorylation of CIN85 that subsequently influences EGFR ubiquitination
Hsieh et al., Toxicol In Vitro 2013 (Breast Neoplasms...) : These findings suggest that NFD inhibited the EGF induced invasion and migration of MDA-MB-231 cells via EGFR dependent PI3K/Akt signaling, leading to the down-regulation of MMP-9 expression