IndraLab

Statements

AE binds USP13. 7 / 7
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"In HCT15 cells, USP13 overexpression increased DNA synthesis, but the USP13-AE mutant did not (Fig.  xref g)."
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"Knockdown of USP13 increased MKK3 ubiquitination (Fig.  xref a), and wild-type USP13, but not the catalytically inactive USP13-AE mutant, effectively reduced this modification (Fig.  xref b)."
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"In HCT116 cells, USP13 overexpression enhanced migration, but the USP13-AE mutant did not (Fig.  xref i)."
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"To determine whether USP13 contributes to malignant phenotypes, we established HCT116 and HCT15 cell lines stably overexpressing wild-type USP13 (USP13-WT) or its catalytically inactive mutant USP13-AE (C345A/M664/739E) (Fig.  xref a), and generated USP13-knockout RKO and SW48 cells via CRISPR/Cas9 (Fig.  xref b)."
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"Furthermore, The interaction was dependent on USP13 catalytic activity, as the USP13-AE mutant displayed reduced binding (Fig.  xref g)."
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"USP13 overexpression promoted colony formation, whereas the USP13-AE mutant had no such effect (Fig.  xref e-f)."
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"Moreover, CHX chase assay demonstrated that overexpression of wild-type USP13, but not the USP13-AE mutant, resulted in an extension of MKK3's half-life and a delay in its degradation (Fig.  xref k)."
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