IndraLab

Statements


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"The deacetylation of USP39 by SIRT7 promotes the stability and thereby accelerates cell proliferation and tumorigenesis of HCC [10] ."

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"To further examine how USP39 promotes tumorigenesis in vivo, tumor and para-tumor tissues collected from Usp39 and WT mice were analyzed by transcriptome sequencing."

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"Growing evidence indicates that abnormal expression of USP39 contributes to tumorigenesis and is linked to HCC progression ."

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"USP39 promotes tumorigenesis by stabilizing and deubiquitinating SP1 protein in hepatocellular carcinoma ."

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"USP39 promotes tumorigenesis partially through a splicing switch of KANK2."

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"An increasing amount of evidence has demonstrated that the aberrant expression of USP39 promotes tumorigenesis and is associated with HCC progression [13, 14]."

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"The de-acetylation of USP39 by SIRT7 can promote its stability and thereby accelerate HCC cell proliferation and tumorigenesis."

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"et al. have reported that overexpression of USP39 predicts poor prognosis and promotes tumorigenesis of prostate cancer [7] ."

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"In HCC, SIRT7-mediated deacetylation impedes MYST1-facilitated acetylation of USP39, which is a prerequisite for its E3 ligase-induced degradation [55] and accelerates the tumorigenesis of HCC."

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"To elucidate the underlying mechanism of USP39-mediated tumorigenesis of PC, we examined the activation of multiple signaling pathways."

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"USP39 promotes hepatocellular carcinogenesis through regulating alternative splicing in cooperation with SRSF6/HNRNPC."