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EGFR phosphorylates PTK2. 23 / 25
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"When combining NIR-PTT with anti-EGFR-GNs in EGFR positive MDA-MB-231 cells and tumors, we observed obstruction of the EGFR mediated intracellular signal pathway (low phosphorylated mTOR, AKT, ERK1/2 and FAK levels) involved in cell proliferation and survival, as well as strong anti-proliferative (low Ki-67 level) and apoptotic activity (high cleaved caspase-3 and TUNEL levels)."
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"In order to study phosphorylation of FAK by EGF-R and alphavbeta3 activation, we determined p-FAK expression levels as a function of alphavbeta3/VN interaction and EGF-R activation by EGF."
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"FAK can be transphosphorylated by activated EGFR, and FAK function is required for EGF stimulated chemotaxis and motility [XREF_BIBR]."
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"Eighteen hours after scrape wounding, addition of HB-EGF significantly increased relative protein levels of p-FAK (1.42 +/- 0.05 vs. 1.00 +/- 0.01, p = 0.019), whereas blocking of EGFR activity with AG1478 inhibited the expression of p-FAK (0.83 +/- 0.08 vs. 1.00 +/- 0.01, p = 0.046) and also abolished HB-EGF-induced phosphorylation of FAK (0.93 +/- 0.07 vs. 1.42 +/- 0.05, p = 0.025) (XREF_FIG)."
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"RhoA-GTP-transfected cells showed a cortical array of F-actin, rounded morphology, reduced spreading potential and a dephosphorylation of FAK that was released by integrin dependent fibronectin adhesion and a specific EGFR tyrosine kinase inhibitor."
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"Another finding of our study was the observation that CD73 enhanced invasion and metastasis of HNSCC cells, mediated by activation of EGF and EGFR signaling, and its downstream phosphorylation of FAK."
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"Importantly, we have also demonstrated that Egfl7 could promote the metastasis of HCC by enhancing cell motility through EGFR-dependent FAK (focal adhesion kinase) phosphorylation [ xref ]."
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"This study demonstrated that EGF/EGFR can phosphorylate FAK and induce EMT in colorectal cancer cells.As knowledge of miRNAs continues to grow, more than 1,000 miRNAs have been identified in human gene banks."
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"However, treatment of the cells with PF573228 and a pharmacological inhibitor of EGFR, gefitinib, abrogated RCP induced EGFR, and FAK phosphorylation, respectively."
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"Another research reported that heterodimerization of proMMP-9 with CD44 can activate EGFR, which leads to phosphorylation of its downstream effectors ERK, AKT, and FAK and favors cell migration and invasion."
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"The EGF receptor (EGFR) inhibitor also suppressed 17-PT-PGE2-upregulated FAK phosphorylation."
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"We also noticed that 0.01-0.3 microM defactinib treatment in H292 cells induced paradoxical increases in FAK pY397 that were in alignment with increases in pEGFR, suggesting that FAK-kinase inhibition led to FAK hyperphosphorylation by EGFR."
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"HER2 and EGFR phosphorylate kinase-dead FAK to maintain cell migration and invasion."
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"We show that FAK positioned between ILK and EGFR activates EGFR, which in turn phosphorylates FAK, leading to a positive feedback loop in RCP induced ovarian cancer cell invasion."
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"HER2 and EGFR phosphorylate kinase-dead FAK to maintain cell migration and invasion."
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"Finally the C. pneumoniae infection leads to FAK1 activation XREF_BIBR, and it is conceivable that EGFR activation by Pmp21 induces phosphorylation of FAK, which also is involved in cytoskeleton regulation."
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"The EGF receptor (EGFR) inhibitor also suppressed 17-PT-PGE2-upregulated FAK phosphorylation."
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"Given these findings, HER2 promotes EGFR phosphorylation and Smad3 phosphorylation, which contribute to Fak phosphorylation leading to EMT."
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"We also noticed that 0.01–0.3µM defactinib treatment in H292 cells induced paradoxical increases in FAK pY397 that were in alignment with increases in pEGFR, suggesting that FAK-kinase inhibition led to FAK hyperphosphorylation by EGFR."
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"However, FAK phosphorylation was abrogated by EGFR inhibition."
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"Collectively, our study shows for the first time that overexpression of Egfl7 in HCC and Egfl7 promotes metastasis of HCC by enhancing cell motility through EGFR-dependent FAK phosphorylation."
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"We show that FAK positioned between ILK and EGFR activates EGFR, which in turn phosphorylates FAK, leading to a positive feedback loop in RCP-induced ovarian cancer cell invasion."
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"Mechanistically, de4 EGFR significantly upregulated the extracellular regulated protein kinase, AKT, focal adhesion kinase (FAK) and Src phosphorylation and matrix metalloproteinase-9 expression while downregulated the expression of E-cadherin."
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