IndraLab

Statements


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"OTUB1 exacerbated CRC malignancy by promoting the protein stability β-Catenin through inhibition of UPP pathway induced β-Catenin protein degradation."

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"Meanwhile, the expression of NDUFS2 was overexpressed significantly after being transfected with OE-NDUFS2 plasmid, but the overexpression was abolished by co-transfection with sh-OTUB1 plasmids (Fig. 6D), suggesting that OTUB1 could promotes the expression of NDUFS2.To further test that whether OTUB1 could promote NDUFS2 protein degradation, MG132, chloroquine and CHX assay were used."

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"We had previously demonstrated that human Otub1 protein leads to degradation of human GRAIL protein, and in a similar manner, murine Otub1 protein leads to murine GRAIL protein degradation (supplemental Fig. 3).4 Ex vivo isolated naive CD4 T cells express no Otub1 protein, thus allowing GRAIL expression (XREF_FIG, first lane), despite the presence of detectable Otub1 mRNA as mTOR mediated protein translation is inactive in these cells."

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"Together, these results show that the protein abundance of CCN6 is enhanced by OTUB1, which possibly inhibits CCN6 protein degradation rather than augmenting its production.3.2 OTUB1 stabilizes CCN6 protein by reducing K48 ubiquitination."