Gene interactions and pathways from curated databases and text-mining

◀ Back to EGFR

EGFR — IFI44

Text-mined interactions from Literome

Takeyama et al., J Immunol 2000 (MAP Kinase Signaling System) : Exogenous hydrogen peroxide and neutrophils activated by IL-8, FMLP, or TNF-alpha increased EGFR tyrosine phosphorylation and subsequent activation of p44/42mapk and up-regulated the expression of MUC5AC at both mRNA and protein levels in NCI-H292 cells ... Neutrophil supernatant induced EGFR tyrosine phosphorylation, activation of p44/42mapk , and MUC5AC synthesis were inhibited by antioxidants ( N-acetyl-cysteine, DMSO, dimethyl thiourea, or superoxide dismutase ) ; neutralizing Abs to EGFR ligands ( EGF and TGF-alpha ) were without effect, and no TGF-alpha protein was found in the neutrophil supernatant ... In contrast, the EGFR ligand, TGF-alpha, increased EGFR tyrosine phosphorylation, activation of p44/42mapk , and subsequent MUC5AC synthesis, but these effects were not inhibited by antioxidants
Xie et al., Eur J Biochem 2002 : The signaling pathways that are rapidly elicited by the interaction of ouabain with Na ( + ) /K ( + ) -ATPase, and are independent of changes in intracellular Na ( + ) and K ( + ) concentrations, include activation of Src kinase, transactivation of the epidermal growth factor receptor by Src, activation of Ras and p42/44 mitogen activated protein kinases, and increased generation of reactive oxygen species by mitochondria
Lui et al., Oncogene 2003 (Carcinoma, Squamous Cell...) : In HNSCC cells that express elevated levels of both GRPR and EGFR, we found that GRP induced rapid phosphorylation of EGFR as well as p44/42-MAPK activation ... Using several EGFR-specific tyrosine kinase inhibitors and cells derived from EGFR knockout mice, we demonstrated that GRP induced p44/42-MAPK activation was dependent upon EGFR activation
Li et al., J Biol Chem 2005 : Tyrosine phosphorylation of Srcasm is dependent on growth factors and the activity of EGFR and SFKs. Increased Srcasm expression enhances p44/42 mitogen activated protein kinase activity and Elk-1 dependent transcriptional events
Nkabyo et al., Am J Physiol Gastrointest Liver Physiol 2005 (MAP Kinase Signaling System) : Inhibitors of EGFR ( AG1478 ) and p44/p42 MAPK ( U0126 ) phosphorylation blocked redox dependent p44/p42 phosphorylation, indicating that signaling occurred by EGFR
Wu et al., Diabetologia 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
Lee et al., American journal of physiology. Renal physiology 2008 : In addition, the PKC inhibitors or an EGFR inhibitor ( AG-1478 ) blocked the BSA induced phosphorylation of p44/42 mitogen activated protein kinases ( MAPKs )