IndraLab
Statements
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"Another point of interest is the fact that the two partners in the well-known bidirectional activatory trans-phosphorylation between EGFR and Src, where Src phosphorylates the EGFR [ xref – xref ], and the EGFR phosphorylates Src [ xref ], are regulated by CaM, albeit in different manners."
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"NT also induced a time-dependent increase in EGFR Tyr(845) phosphorylation and phosphorylation of c-Src and signal transducer and activator of transcription 5b (Stat5b) (a downstream effector of Tyr(845)), events that were blocked by specific inhibition of c-Src (which mediates Tyr(845) phosphorylation of EGFR) or of EGFR."
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"Another point of interest is the fact that the two partners in the well-known bidirectional activatory trans-phosphorylation between EGFR and Src, where Src phosphorylates the EGFR [XREF_BIBR - XREF_BIBR], and the EGFR phosphorylates Src [XREF_BIBR], are regulated by CaM, albeit in different manners."
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"Src can also be directly phosphorylated by EGFR [XREF_BIBR], and as FAK is recruited to sites of integrin clustering and is required for growth factor stimulated motility, Src is likely involved in the cooperativity or crosstalk between growth factor and integrin signaling [XREF_BIBR]."
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"Thus, activation of the gintonin-biotin conjugate-mediated LPA receptor transactivates the EGF receptor via c-Src phosphorylation and activated EGF receptor is also coupled to ERK activation, resulting in cell migration that is blocked by the EGF receptor inhibitor (Fig. 6).4
Discussion."
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"Consistently, the molecular analyses of the PP121- or SC-1–treated tumors revealed a reduction in the phosphorylation of multiple growth factors signaling proteins, including the phosphorylation of Src family kinases, EGFR, and FAK compared with vehicle-treated controls (SI Appendix, Fig. S5B)."
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"The association of Rap1 in the modulation of EGFR level, its signaling pathway and pathological condition such as PE and FGR would be considered in our subsequent study.In conclusion, Rap1 functions as a mediator of EGF/HB‐EGF‐induced AKT, ERK1/2, p38MAPK, and Src phosphorylation via the EGFR signaling pathway and is a posttranscriptional modulator of EGFR during EVT invasion."
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"It should be noted that Src can induce activation of EGFR by direct phosphorylation on Tyr-845. xref An experimental study with a mutation of EGFR at Tyr845 found that Tyr845 is essential for EGF-induced DNA synthesis in murine fibroblasts. xref This experiment also demonstrated that Src dependent EGFR phosphorylation (Tyr845) is required for DNA synthesis induced by G protein-coupled agonists (endothelin and LPA), cytokines, and growth hormone in murine fibroblasts. xref In addition, over-expression studies in tumor cell lines revealed that c-Src-induced tyrosine phosphorylation of EGFR at 845 is required for the mitogenic and malignant properties of EGFR. xref These findings indicate that Src-dependent phosphorylation at Tyr845 is essential for EGFR to exert its cellular functions."
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"Src can also be directly phosphorylated by EGFR [ xref ], and as FAK is recruited to sites of integrin clustering and is required for growth factor-stimulated motility, Src is likely involved in the cooperativity or crosstalk between growth factor and integrin signaling [ xref ]."