IndraLab

Statements


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"The increase in USP7 in Osterix-Cre(+); Kcnma1f/f mice might stabilize the function of Axin1, which promoted the degradation of β-catenin in osteoblasts (Fig. 6)."

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"USP7 represses Wnt and beta-catenin signaling through stabilization of Axin, which is a part of the destruction complex that inhibits beta-catenin."

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"Upon Wnt3a treatment, knockout of Usp7 increased Wnt3a-induced accumulation of active β-catenin in C3H10T1/2 cells (Fig. 5a)."

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"In the presence of ODM, genetic knockout or pharmacological inhibition of USP7 in C3H10T1/2 and ST2 cells increased the alkaline phosphatase staining (Fig. 5f) and mRNA expression of Alpl and β-catenin target genes (Fig. 5g), which were blocked by WNT974 (Fig. 5f, g)."

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"Ji et al. demonstrated that USP7 can stabilize AXIN1, a key protein in the Wnt pathway, and increase the degradation of β-catenin in osteoblasts, thus participating in the regulation of osteogenic differentiation [30]."

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"USP7 inhibits Wnt/beta-catenin signaling through promoting stabilization of Axin."

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"USP7 inactivation decreases half-life of GSK3beta and beta-Catenin proteins."

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"Knockout Usp7 using independent gRNAs enhanced Wnt3a-induced accumulation of active β-catenin (Fig. 6a)."

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"Ectopic expression of wild-type USP7 strongly suppressed Wnt3a-induced STF reporter and β-catenin accumulation (Fig. 1h and Supplementary Fig. 1g)."

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"Similarly, USP7 stabilizes the scaffold protein AXIN, promotes the complex destroyed by β-catenin (APC-AXIN-GSK-3 β), promotes the degradation of β-catenin, and maintains a very low concentration in normal cells, which results in inhibition of Wnt signal transduction and osteoblast formation [30,41]."

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"Consistently, knockout of USP7 enhanced Wnt3a-induced accumulation of active β-catenin in HEK293T cells (Fig. 1c)."