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UCHL3 activates CTNNB1. 8 / 8
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"Accordingly, UCHL3 deficiency decreased the CTNNB1 protein half-life (Fig. 5H)."
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"Taken together, UCHL3 promotes the stability of CTNNB1, and this effect depends on its deubiquitinating activity."
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"Our results suggest that UCH-L3 induces the stabilization of beta-catenin, which is required to promote stemness during autophagy activation."
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"We further speculated that ubiquitin C-terminal hydrolase-L3 (UCH-L3), the deubiquitinase formerly reported to maintain stem cell properties, could activate β-catenin signaling during autophagy (Lee et al., 2021; Ouyang et al., 2020)."
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"In addition, the knockdown of endogenous UCH-L3 abrogated the upregulation of β-catenin induced by glucose deprivation (Supplementary Fig. S2B)."
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"UCHL3 increases β-catenin protein stability via removing K48-specific poly-ubiquitin chains from β-catenin protein."
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"In general, our results indicates that UCHL3 increases the stability of β-catenin, which in turn facilitates tumorigenesis of HCC, suggesting that targeting UCHL3 may be a promising approach for the treatment of HCC."
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"However, it is possible that β-catenin signaling activated by UCH-L3 is required to maintain the stem cell properties of GCSCs during autophagy-activating conditions, such as nutrient deprivation.In summary, we suppose that the suppression of UCH-L3 could effectively limit gastric cancer recurrence after surgery by preventing GCSC induction."
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