IndraLab

Statements

USP4 activates apoptotic process. 8 / 9
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"Moreover, knockdown of USP4 could significantly inhibit cell proliferation and increase cell apoptosis in U87 and T98G cells."
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"However, in response to cisplatin induced stress, the knockdown of USP4 could markedly increase the apoptotic rate of melanoma cells, and USP4 deficiency sensitized melanoma cell to cisplatin induced apoptosis by activating p53 pathway."
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"USP4 knockout mice exhibited exacerbated hepatic I/R injury, as evidenced by enhanced liver inflammation via the NF-kappaB signalling pathway and increased hepatocyte apoptosis."
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"Consistent with this, the results of Hou et al. 28 showed that USP4 promotes apoptosis and inhibits NF-kappaB activation in head and neck squamous cell carcinoma."
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"The findings showed that the expression of TGF-betaR1 and USP4 were increased in hypertrophic scar tissues and fibroblasts, and that down-regulating USP4 inhibited hypertrophic scar fibroblast proliferation and migration and induced cell apoptosis in vitro."
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"However, in response to cisplatin treatment, USP4 deficiency significantly augmented melanoma cells apoptosis by activating p53 signalling."
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"We subsequently showed that USP4 regulated cisplatin induced cell apoptosis via p53 signalling."
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"USP4 might negatively regulates RIP1-mediated NF-κB activation and promotes TNF-α-induced apoptosis in FaDu cells, as well as directly interacted with receptor-interacting protein 1 (RIP1) and deubiquitinated K63-linked ubiquitination from RIP142."
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