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"These data indicate that EGF stimulates active ERK in a time- and concentration dependent manner in freshly isolated pGCs and that this experimental approach represents an effective manner with which to evaluate the role of EGF and the ERK signal transduction pathway in freshly harvested pGC."
"We previously reported a relationship between the ambivalent activity of EGF and the p42-mitogen-activated protein (MAP) kinase activity. Thus, 10(-12) M EGF induced a sustained MAP kinase activation, whereas 10(-9) M EGF led to a sharp, but transitory, activation. The MAP kinases are activated by MAP kinase kinases (MEK1 and MEK2)."
"EGF also prevented H2O2-induced disruption of the actin cytoskeleton and the dissociation of occludin and ZO-1 from the actin-rich detergent-insoluble fractions. MEK (MAPK/ERK kinase, where ERK stands for extracellular signal related kinase) inhibitors, PD98059 and U0126, completely blocked these protective effects of EGF on TJs. EGF rapidly increased the levels of phosphorylated MEK (p-MEK) in detergent-soluble fractions and phosphorylated ERK (p-ERK) in detergent-insoluble fractions. p-ERK was colocalized and co-immunoprecipitated with occludin. "
"senescence-like growth arrest was accompanied by impaired activation of mitogen-activated protein kinase (MAPK) pathways, namely, extracellular-regulated protein kinase, c-jun N-terminal kinase and p38 MAPK, in response to epidermal growth factor (EGF) and insulin-like growth factor-I (IGF-I)"
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"In RTCs, binding of EGF to EGFR stimulates activities of ERK, phospholipase C (PLC), and SphK, resulting in increased intracellular levels of S1P, while the EGF and EGFR mediated Ca 2+ mobilization, which may regulate apoptosis, requires activation of PLC and SphK in HEK293 cells [XREF_BIBR]."