IndraLab

Statements

USP22 activates mTORC1. 7 / 7
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"In summary, USP22 activates mTORC1 by deubiquitinating FKBP12.2.5 Activated mTORC1 further inhibits the autophagic degradation of USP22."
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"In addition, USP22 activated mTORC1 by deubiquitinating FK506‐binding protein 12 (FKBP12) and activated mTORC1, in turn, further stabilizing USP22 by inhibiting autophagic degradation."
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"Therefore, high USP22 expression in tumor tissues could predict the benefit of sirolimus in patients with HCC after LT, which supports the significant role of USP22 in activating mTORC1 in HCC.In summary, in HCC, USP22 overexpression increased mTORC1 activity and sensitized HCC toward rapamycin."
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"Mechanistically, USP22 interacted with FKBP12 to activate the mTORC1 pathway through deubiquitylation."
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"These results further validated that the tumors with Usp22 overexpression were significantly larger and more aggressive than those in the control group, whereas Usp22 ablation diminished this effect.2.2 USP22 activates the mTORC1 signaling pathway."
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"In summary, USP22 activates mTORC1 by deubiquitinating FKBP12."
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"Because USP22 was shown to activate mTORC1 activity, we hypothesized that USP22 interacts with certain proteins associated with mTORC1, including regulatory‐associated protein of mTOR (Raptor), mTOR‐associated protein, LST8 homolog (MLST8), mTOR, and FK506‐binding protein 12 (FKBP12)."
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