IndraLab

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USP10 activates PTEN. 11 / 11
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"The deubiquitinase USP10 restores PTEN activity and inhibits non-small cell lung cancer cell proliferation."
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"In contrast to TRIM25, USP10 restored PTEN phosphatase activity and reduced the production of the secondary messenger phosphatidylinositol-3,4,5-trisphosphate, thereby inhibiting AKT/mammalian target of rapamycin progrowth signaling transduction in NSCLC cells."
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"Our aforementioned studies have shown that USP10 restores the phosphatase activity of PTEN, thereby inhibiting the AKT/mTOR signaling."
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"By countering TRIM25, USP10 rescues PTEN phosphatase activity and reduces the production of PI(3,4,5)P3 in NSCLC cells, therefore inactivating the AKT/mTOR signaling pathway in NSCLC cells (Fig. 5)."
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"These data thus demonstrated that USP10 might activate PTEN, thus inhibiting the AKT/mTOR signaling pathway."
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"Given that TRIM25-mediated K63-linked ubiquitination does not alter PTEN stability (10), and USP10 prevents PTEN from K63-linked polyubiquitination mediated by TRIM25, we wondered whether PTEN stability was modulated by USP10."
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"Specifically, USP10 activates PTEN by preventing its K63-linked polyubiquitination mediated by TRIM25 and suppresses the AKT/mammalian target of rapamycin signaling pathway, thereby inhibiting NSCLC proliferation, indicating that it may be a potential drug target for cancer treatment."
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"These data thus demonstrated that USP10 might activate PTEN, thus inhibiting the AKT/mTOR signaling pathway."
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"Moreover, although it is downregulated in NSCLC cells, restoration of USP10 can activate PTEN, therefore decreasing the production of PI(3,4,5)P3 and suppressing the AKT/mTOR signaling transduction and inhibiting NSCLC cell proliferation and migration."
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"Finally, USP10 influences the AKT signaling pathway and activates phosphatase and tensin homolog (PTEN) by blocking its K63-linked polyubiquitination, which in turn suppresses the growth of NSCLC [ xref , xref ]."
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"Specifically , USP10 activates PTEN by preventing its K63-linked polyubiquitination mediated by TRIM25 and suppresses the AKT / mTOR signaling pathway thereby inhibiting NSCLC proliferation , indicating that it may be a potential drug target for cancer treatment ."
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