"On the other hand, up-regulation of EGFR has been observed to activate AKT1 XREF_BIBR."
"Activation of EGFR triggers three main signaling pathways : the ERK pathway, the PI3K and protein kinase B (Akt) pathway, and the Jakus kinase (JAK)/signal transducer and activator of transcription protein (STAT) pathway."
"In future studies, it will be important to elucidate the precise mechanism by which PI3K-Akt-1 activation by EGFRvIII might promote DNA-PKcs hyperactivation in GBM tumor cells."
"We observed that inhibition of EGFR kinase activity with AG1478 significantly attenuated H2O2 induced p38 (SAPK) and ERK1/2 activation, but did not inhibit Akt1 activation."
"Because AKT1 can be activated by the EGFR signaling to enhance cancer cell survival, it is possible that the AKT1 activity may be further exaggerated due to the augment of both EGFR and AKT1 gene copy numbers and result in a worse 5-year OS than patients with an increase in EGFR gene copy numbers alone."
"Inhibition of EGFR activation by novel small molecules or by short hairpin RNA knockdown in Ang II treated SV40 mesangial cells in vitro suppresses protein kinase B and extracellular signal related kinase signaling pathways and transforming growth factor-beta and Sma- and Mad related protein activation, and abolishes the accumulation of fibrotic markers such as connective tissue growth factor, collagen IV."
"Previous studies indicated that EGFRvIII expressing cells constitutively activate phosphatidylinositol 3-Kinase (PI3-K) and Akt1, and that Akt1 can inhibit HRR by inducing cytoplasmic retention of Rad51."
"In summary, these studies indicate that EGF signaling through EGFR activates PKBalpha and AKT as a principal target, and blocking this pathway with the EGFR specific tyrosine kinase inhibitor, Iressa, results in programmed cell death."
"Moreover, while ligand-activated EGFR stimulates both the RAS-RAF-MAPK and PI3K-Akt-1 pathways ( xref ), EGFRvIII preferentially activates PI3K-Akt-1 ( xref , xref )."
"Here we show that cholesterol depletion by beta-cyclodextrin disrupts caveolae structure and concomitantly inhibits tyrosine phosphorylation of the EGF-R and subsequent activation of protein kinase B (PKB)/Akt induced by angiotensin II."