IndraLab

Statements

SQSTM1 binds USP20. 13 / 13
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"This is the first report that reveals the molecular mechanism of the USP20-p62 axis regarding NF-κB-mediated cell survival."
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"Immunoprecipitation assays supported the endogenous interactions between USP20 and p62 upon TNFα treatment in HeLa cells ( xref B)."
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"These findings strongly suggest that the USP20-p62 axis plays an essential role in NF-κB-mediated cell survival induced by the TNFα-atypical PKCζ signaling pathway."
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"Our finding that USP20 stabilizes the p62 protein prompted us to examine whether USP20 directly binds to p62."
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"USP20 specifically binds to p62 and acts as a positive regulator for NF-κB activation by TNFα through deubiquitinating lysine 48 (K48)-linked polyubiquitination, eventually contributing to cell survival."
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"Based on this speculation, our current experiments provide evidence that the p62-USP20 axis is required for PKCζ-mediated NF-κB activation upon TNFα treatment."
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"This time point coincided with the timing of endogenous p62 interaction with USP20 ( xref B)."
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"Co-immunoprecipitation assays revealed the direct interaction of USP20 with p62 when plasmids encoding HA-USP20 and Flag-p62 were ectopically expressed in HeLa cells ( xref A)."
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"Based on this finding, we next examined the endogenous interaction of USP20 with p62 upon TNFα treatment."
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"Herein, we find that USP20 binds to p62 at 5 min upon TNFα treatment and thus stabilizes it through removing the lysine 48 (K48)-linked polyubiquitin chains."
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"Because our results suggest that the USP20-p62 axis is responsible for PKCζ-mediated NF-κB activation for cell survival, USP20 depletion may promote cell death."
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"USP20 specifically binds to p62 and acts as a positive regulator for NF-kappaB activation by TNFalpha through deubiquitinating lysine 48 (K48)-linked polyubiquitination, eventually contributing to cell survival."
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"We speculate that the USP20-p62 axis works on the upstream of RIPK1 in non-classical PKCζ-mediated NF-κB activation upon TNFα treatment and USPS20 depletion decreases p62 scaffolding activity, resulting in the release of RIPK1."
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