IndraLab
Statements
sparser
"Mechanistically, we demonstrated that rLZ-8 bound to EGFR to induce EGFR autophosphorylation at tyrosine1045 and trigger ubiquitination by inducing the formation of EGFR/Cbl complexes, resulting in the degradation of EGFR; however, Cbl-shRNA abolished rLZ-8-induced EGFR degradation."
rlimsp
"In controls, autophosphorylation of EGFR at both pY1068 and pY1045 peaked at 5 min but was reduced by 15 min after EGF stimulation (Figure 3A), whereas in Gαs-depleted cells EGFR autophosphorylation at these sites was increased greater than threefold at both 5 and 15 min after ligand stimulation (Figure 3, A and B)."
sparser
"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."
rlimsp
"ERK(1/2) phosphorylation by Src activation depended on β-arrestin 2, but not β-arrestin 1, was accompanied by Src/EGFR co-precipitation and phosphorylation of the EGFR at the Src-phosphorylated Y845 site and the Y1045 autophosphorylation site; it was independent of transactivation but dependent on MAPK/ERK kinase activity, suggesting EGFR phosphorylation independently of the receptor-tyrosine kinase or activation of Ras or Raf directly from Src."
trips
"Mechanistically, we demonstrated that rLZ-8 bound to EGFR to induce EGFR autophosphorylation at tyrosine1045 and trigger ubiquitination by inducing the formation of EGFR/Cbl complexes, resulting in the degradation of EGFR; however, Cbl-shRNA abolished rLZ-8-induced EGFR degradation."
rlimsp
"Mechanistically, we demonstrated that rLZ-8 bound to EGFR to induce EGFR autophosphorylation at tyrosine1045 and trigger ubiquitination by inducing the formation of EGFR/Cbl complexes, resulting in the degradation of EGFR; however, Cbl-shRNA abolished rLZ-8-induced EGFR degradation."
sparser
"Although further work is needed to define the precise molecular mechanisms of EGFR internalization and degradation, the accumulated evidence suggests the following model of EGF-induced EGFR endocytosis: EGFR that is autophosphorylated at Y1045 within its C-terminal domain recruits and interacts with the TKB domain of c-Cbl."