IndraLab

Statements

EGFR activates phosphorylated AKT. 19 / 19
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"Inhibition of EGFR activity using cetuximab partially abrogated the feedback activation of phosphorylated receptor tyrosine protein kinase erB-3 (p-HER3) and p-AKT serine/threonine kinase (AKT), as well as prevented reactivation of p-extracellular regulated kinase (ERK) conferred by AZD6244 treatment."
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"The in vivo assay demonstrated that EGFR and SOS1 promoted growth of nuclear p-AKT +, Bcl-2 + cells results in the resistance of hepatoma cells to ASPP2 and p53 complex induced apoptosis and that blocking nuclear translocation of EGFR dramatically improves and enhances the pro apoptotic function of ASPP2."
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"Co-culture with MRC-5 cells did not protect HCC827 cells from gefitinib induced pEGFR inhibition but significantly increased p-Akt and p-ERK activation compared with the mono-culture cells."
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"However, in the absence of mutated HRAS, other upstream signaling molecules can also drive EGFR independent stimulation of p-AKT and p-MAPK and lead to erlotinib resistance as well."
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"The transfection of EGFR alone with EGF increased p-Akt modestly."
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"These results recapitulated our in vitro observations using SNB19 and LN444 cells, further suggesting that PKA induced p-S of Dock180 is critical for EGFRvIII stimulated p-Akt, p-Erk1/2, Rac1 activity and cell migration in glioma cells."
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"The results showed that inhibition of EGFR with erlotinib in breast cancer MDA-MB-231 and HBL100 cell lines significant downregulated p-AKT, p-ERK, CD44, KLF4, Myc, Slug and Snail in these cells (XREF_FIG)."
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"In addition, we searched for ser473 p-Akt (p-Akt), which is activated by EGFR, and Epithelial Membrane Antigen (EMA), which is generally used as differential diagnosis marker of mesothelial cells."
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"In addition, we searched for ser473 p-Akt (p-Akt), which is activated by EGFR, and Epithelial Membrane Antigen (EMA), which is generally used as differential diagnosis marker of mesothelial cells."
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"Our above results showed the gefitinib and PA-MSHA could suppress EGFR mediated p-AKT and p-ERK pathway in three lung cancer cell lines, including A549."
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"In present study, we found that co-inhibition of EGFR and IGF-1R could completely abolished the p-Akt and p-Erk1/2 and resulted in a synergistic radiosensitizing effect in MDA-MB-468 cells."
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"In addition, silencing of MET caused an upregulation of EGFR and p-AKT, which was abrogated by concomitant silencing of MET and EGFR in CMM cells resistant to MAPK targeting drugs."
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"A previous report suggested that loss of TIP30 improves EGFR activity, which leads to upregulated p-AKT and pERK1/2 in human lung adenocarcinoma and mammary tumours."
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"Dual targeting of EGFR and ErbB3 most effectively blocked p-Erk and p-Akt in the presence of EGFR ligands and HRG, which translated into synergistic inhibition of tumor growth in A549 (XREF_FIG) and H322 (XREF_FIG)."
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"In addition to STAT3, p-ERK1/2 and p-AKT can also be activated by EGFR; accordingly, we investigated whether these additional downstream effectors of p-EGFR signaling were reduced in 1,3,4-O-Bu 3 ManNAc treated cells."
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"As shown in XREF_FIG, when compared to the vector control, expression of Dock180 WT had a minimal impact on EGFRvIII stimulated p-Akt, p-Erk1/2 and Rac1 activity whereas expression of Dock180 S1250L attenuated EGFRvIII stimulation of p-Erk1/2 and Rac1 activity but had no effect on p-Akt."
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"Interestingly, we found no effects on the levels of phosphorylated PKB and Akt, which can also be activated by EGFR signalling via phosphatidylinositol 3 '-kinase, the cyclin dependent kinase inhibitor p27 or the proliferation marker Ki67."
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"RAS is capable of activating both the PI3K and AKT and MAPK, and activating mutations in RAS could explain EGFR independent stimulation of p-AKT and p-MAPK."
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"Consistent with these data, ectopic expression of a PKA inhibitor (PKI) 21 also reduced EGFRvIII promoted p-S of Dock180, p-Erk1/2, p-Akt, Rac1 activity, cell migration and cell proliferation of SNB19 and LN444 glioma cells (XREF_FIG and data not shown)."
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