IndraLab
Statements
reach
"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)."
reach
"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)."
"In this study, we demonstrate that growth factor receptors including hepatocyte growth factor receptor met, epidermal growth factor receptor, and platelet-derived growth factor receptor directly phosphorylate fak on tyr194 in the ferm domain collectively, this study provides the first example to explain how fak is activated by receptor tyrosine kinases."
reach
"The activated EGFR signals through phosphorylated tyrosine residues to stimulate multiple pathways, including mitogen activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/Akt, signal transducers and activators of transcription (STAT), phospholipase C, and Src and focal adhesion kinase (Src and FAK) pathways."
"In this study, we demonstrate that growth factor receptors including hepatocyte growth factor receptor met, epidermal growth factor receptor, and platelet-derived growth factor receptor directly phosphorylate fak on tyr194 in the ferm domain collectively, this study provides the first example to explain how fak is activated by receptor tyrosine kinases."
"CCh also induced association of FAK with the EGFr and FAK phosphorylation was attenuated by an EGFr inhibitor, tyrphostin AG1478, and an inhibitor of Src family kinases, PP2. The actin cytoskeleton disruptor, cytochalasin D (20 microM), abolished FAK phosphorylation in response to CCh but did not alter CCh-induced EGFr or ERK MAPK activation. "