IndraLab
Statements
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"EGFR was IPed from the cell lysates and IBed for total EGFR and receptor auto-phosphorylation on Y1173 and Y1068. xref shows that the L858R MT EGFR of H3255 cells is constitutively phosphorylated on Y1173 and Y1068, as expected ( xref ), which is further increased by both EGF and CS treatments, and that Erlotinib treatment could abolish the receptor auto-phosphorylation on Y1173 and Y1068 in control and EGF stimulation conditions."
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"In pancreatic adenocarcinomas, Fibulin-3 binds EGFR (competitive to EGF) causing autophosphorylation of EGFR at Tyr-992 and Tyr-1068 and the subsequent phosphorylation of AKT at Thr-308 and ERK at Thr-202 and Tyr-204 and, thus, accelerates pancreatic adenocarcinoma growth xref ."
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"Treatment of cells from four GBM PDXs with comparable EGFRvIII expression levels ( xref ) and two low background level EGFR expressing and non-activated control GBM PDX cultures with 1 or 10 μM of Gefitinib (reversible Type I), Canertinib (irreversible Type I), Lapatinib (reversible Type II) and Neratinib (irreversible Type II) led to similar levels of EGFR kinase activity inhibition (up to >90%) as measured by the levels of EGFR autophosphorylation at Y1068 in cells from EGFRvIII-positive PDXs but not in the controls ( xref , xref )."
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"However, they also found that overexpression of Neu1 using recombinant adenovirus (Ad) encoding FLAG-tagged human NEU1 (Ad-NEU1) diminished EGF-stimulated EGFR Tyr-1068 autophosphorylation by up to 44% but instead, enhanced MUC1-dependent Pseudomonas aeruginosa adhesion by about 2-fold and flagellin-stimulated ERK1/2 activation by nearly 2-fold."
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"Mechanistically, FBLN7 binds to the epidermal growth factor receptor (EGFR) through its EGF-like domain, together with the EGF-like calcium-binding domain, and induces EGFR autophosphorylation at tyrosine (Y) 1068 and Y1173, which activates downstream focal adhesion kinase/AKT signaling, thereby leading to fibroblast-to-myofibroblast transdifferentiation."
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"We show that in highly motile GIV-wt cells with an intact GEF motif, EGFR autophosphorylation at Y992, Y1045, and Y1068 and the corresponding adaptor recruitment (PLCγ, cCbl, and Grb2) are enhanced, whereas in rapidly proliferating, GEF-deficient GIV-FA cells these events are suppressed."
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"The results demonstrated that upon 4h's CHMFL-EGFR-26 treatment, the phosphorylation of EGFR Y1068 was inhibited with an EC 50 of 3.6 nM in BaF3-FL-EGFR-L858R -T790M cells and 50 nM in BaF3-TEL-EGFR cells (Figure xref ), suggesting that the drug shows 15-fold selectivity between the EGFR wt and EGFRL858R/T790M. Meanwhile, AZD9291 exhibited similar selectivity between the EGFR wt and EGFR L858R/T790M mutant Y1068 auto-phosphorylation (EC 50 : 63nM and 3.2 nM respectively)."
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"In contrast, blockade or silencing of Src only suppressed EGF-induced EGFR phosphorylation at Y845 but did not affect EGFR autophosphorylation at Y1068 by EGF, indicating that ligand-dependent EGFR phosphorylation at Y845 depends on Src whereas autophosphorylation at other residues such as Y1068 is Src-independent."
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"Moreover, previous study proved that PRMT5‐mediated EGFR Arg1175 methylation positively modulates EGF‐induced EGFR trans‐autophosphorylation at Tyr 1173, but have no effect on EGFR trans‐autophosphorylation at Tyr 1086, 845, 992, 1045 and 1148. xref Herein, we for the first time find that PRMT5 promotes the autophosphorylation of EGFR at Y1068 and Y1172 to activate Akt‐β‐catenin axis in pancreatic cancer cells."
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"The results demonstrated that ibrutinib potently inhibited both EGFR wt/mutant auto-phosphorylation at Y1068. (Fig. xref and xref ) In sensitive cell lines (H1975, PC-9, H3255, HCC827) it also potently inhibited targets downstream of ERK. (Fig. xref and xref ) Interestingly, it significantly affected the phosphorylation of Akt Thr308 and Ser473 in H1975 cells, however not the other three mutant EGFR-expressing cell lines. (Fig. xref , xref ) Although it did not have apparent enzymatic activity against PI3K kinase. ( xref ) This is different from other reported third generation EGFR inhibitors (WZ4002, CO1686 and AZD9291) that can significantly affect the phosphorylation of AktS473 in L858R and del 19 mutant cancer cell lines."