IndraLab

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Mutated USP8 activates EGFR. 10 / 10
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"15 Moreover, USP8 mutations increase its deubiquitinase activity and enhance the stability of EGFR, 16 , 17 which further results in increased mRNA expression level of proopiomelanocortin (POMC), the [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Considering that activation of EGFR-MAPK signaling induces p27 (Kip1) degradation, and p27 (Kip1)-deficient mice develop corticotropinoma XREF_BIBR, XREF_BIBR, we speculate that through activating EGFR signaling USP8 mutation accelerates p27 (Kip1) degradation, representing an important molecular mechanism underlying ACTH hyperproduction (XREF_FIG)."
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"Previous studies have demonstrated that the USP8 mutation causes corticotroph adenomas mainly through activating the EGFR–MAPK signal cascades ."
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"In human corticotroph primary cultures, treatment with the pan-ErbB TKI canertinib as well as the EGFR TKI gefitinib suppresses POMC mRNA, and USP8 mutations, detected in up to two-thirds of CD, may underlie the increase in EGFR signaling in these tumors."
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"Moreover, USP8 mutants induce both EGFR retention on the plasma membrane and recycling of endocytosed EGFR back to the cell surface, causing continuous activation of EGF signaling."
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"The USP8 mutation (14-3-3 somatic mutations) induces corticotroph EGFR adenoma signaling by rescuing EGFR from lysosomal degradation and enhancing EGFR accumulation (9)."
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"As mentioned above, mutations of USP8 prevent EGFR degradation [1]."
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"The USP8 mutation (14-3-3 somatic mutations) inhibits EGFR degradation, enhances EGFR accumulation, and consequently, likely induces corticotroph EGFR tumor signaling."
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"We found that USP8 mutated PAs have a higher incidence of EGFR expression, increased EGFR protein abundance and activation of downstream Erk1/2, indicating that USP8 mutations enhance EGFR signaling in tumors."
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"USP8 mutations prevent EGFR degradation via deubiquitination of EGFR, increase cell surface EGFR expression, and render EGFR as a potential therapeutic target by gefitinib."
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