IndraLab

Statements


USP13 activates MTOR. 8 / 8
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"To confirm USP13 accelerates the proliferation of HCC cells through regulating PRPF6‐AKT‐mTOR signalling, we performed the rescue experiments by silencing PRPF6 in USP13 up‐regulated cells."

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"It was found that knock down of PRPF6 effectively inhibited the cell proliferation and also reduced the expressions of p‐AKT and p‐mTOR induced by overexpression of USP13 (Figures 7A,B)."

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"These results suggest that the USP13‐PRPF6 axis promotes HCC cell proliferation by regulating AKT‐mTOR signalling.3.6 USP13 Expression Is Correlated With PRPF6 in Human HCC Tissues."

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"Overall, USP13 facilitates the malignant progression of HCC cells through the upregulation of WWP1.Thus, we concluded that USP13 stabilized WWP1, and then activated the Akt/mTOR pathway."

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"Further experimental results confirmed that the USP13‐PRPF6 axis promoted the proliferation of HCC cells by modulating the AKT‐mTOR signalling pathway.In conclusion, we have demonstrated that USP13 can decrease the K48/63‐linked polyubiquitination of PRPF6, thereby stabilising this protein and promoting HCC cell proliferation via regulation of the AKT‐mTOR pathway (Figure 8C)."

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"Moreover, USP13 stabilized WWP1 by removing the K29- and K48-linked polyubiquitination chains from WWP1 and then activated the Akt/mTOR pathway in HCC."

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"By acting as an oncogene, USP13 affects HCC malignant progression through the WWP1-mediated Akt/mTOR pathway."

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"Importantly, USP13 modulated the AKT‐mTOR signalling pathway in a manner analogous to PRPF6 (Figures 6D,E)."