IndraLab

Statements



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"Additionally, overexpression of USP49 remarkably inhibits cell proliferation and regulates the PI3K/AKT signal pathway."

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"USP49 loss impairs cell proliferation and leads to aneuploidy."

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"Here, we report that the downregulation of Ubiquitin-specific peptidase 49 (USP49) promotes ferroptosis in OE33 and OE19 cells, thereby inhibiting cell proliferation in vitro and in vivo, whereas the overexpression of USP49 had the opposite effect."

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"Mechanistically, USP49 deubiquitinates and stabilizes FKBP51, which in turn enhances PHLPP 's capability to dephosphorylate AKT Furthermore, USP49 inhibited pancreatic cancer cell proliferation and enhanced cellular response to gemcitabine in a FKBP51-AKT-dependent manner."

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"Mechanistically, USP49 deubiquitinates and stabilizes FKBP51, which in turn enhances PHLPP's capability to dephosphorylate AKT Furthermore, USP49 inhibited pancreatic cancer cell proliferation and enhanced cellular response to gemcitabine in a FKBP51-AKT-dependent manner."

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"USP49 knockout contributes to increased HCT116 cell proliferation and migration."

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"In consistent with this notion, USP49 knockdown was recently reported to result in a decrease of cell proliferation and invasion as well as an increase of cell apoptosis in glioblastoma cells [ 25 ]."

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"As shown in Fig. 6D, overexpression of USP49 significantly inhibited cell proliferation and reversed the promotion effect of miR-5000-3p on cell proliferation ability.Due to USP49 was involved in the PI3K/AKT signaling pathway ."

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"A previous study suggested depletion of USP49 increased pancreatic cancer cell proliferation in vitro, tumorigenesis in vivo, and chemoresistance, proposing that USP49 regulates tumorigenesis and chemoresistance in pancreatic cancer in an AKT-dependent manner ."