IndraLab
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"Thereby, together with these data, it can be concluded that the elevated level of USP8 not only increases the expression of EGFR, PI3K, and P-Akt but also might increase the PI3K and P-Akt expression over EGFR silencing where the PI3K and P-Akt well established the downstream target of EGFR (
Figures 6C, D
)."
"USP8 is known to deubiquitinate EGFR in response to ligand stimulation. USP8 depletion accelerates receptor turnover, whereas loss of hepatocyte growth factor-regulated substrate (Hrs) rescues this phenotype, indicating that USP8 protects EGFR from degradation via an Hrs-dependent pathway. [..]As EGFR stabilization against lysosomal turnover requires deubiquitination by USP8."