IndraLab

Statements

USP35 inhibits apoptotic process. 9 / 9
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"Therefore, endogenous USP35 is not essential for the neuroprotective effects of hUC-MSCs and their EVs in this context.Notably, our study only revealed that overdosed exogenous USP35 encapsulated in hUC-MSC-EVs inhibits apoptosis and mitochondrial damage by stabilizing FUNDC1 in OGD/R-induced SH-SY5Y cells at the cellular level."
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"Collectively, these findings suggest that excessive USP35 enhances the capacity of hUC-MSCs and hUC-MSC-EVs to reduce apoptosis and ROS stress in cocultured SH-SY5Y OGD/R cells."
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"Further functional studies showed that knockdown USP35 expression inhibited cell proliferation and promoted apoptosis."
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"USP35 resists cell apoptosis by stabilizing anti-apoptotic factor BIRC3 and relieves endoplasmic reticulum stress (ERS) by deubiquitinating RRBP1 [20, 22]."
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"Knockdown of USP35 causes reduced proliferation, cell cycle arrest, increased apoptosis, and mitigated migration and invasion of HCC cells."
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"Additionally, USP35 knockdown led to an increased number of cells arrested in the G /G phase (Fig. 3H, I), as well as enhanced apoptosis in HCC cells (Fig. 3J, K)."
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"Strikingly, USP35 overexpression markedly reduced cytotoxic agents-induced cell apoptosis (Fig. 2F, G), while USP35 knockdown led to increased drug-induced cell apoptosis (Fig. S3C, D)."
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"It is possible that USP35 inhibition may synergize with Taxol to induce apoptosis or cell arrest, based on the result that USP35 deficiency itself already leads to multiple mitotic errors, and this outcome could be further exacerbated by Taxol treatment [34]."
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"The results from flow cytometry assays demonstrated that decreased USP35 expression elevated the apoptosis rate of Huh-7 (1.5 vs. 10.1%; Fig. 3E) and Hep3B (1.1 vs. 6.2%; Fig. 3F) cells."
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