IndraLab

Statements

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"The findings that USP15 deficiency promotes T cell activation and cancer cell apoptosis indicated that inhibition of USP15 might suppress tumor growth both via a tumor cell-intrinsic mechanism and by enhancing the anti-tumor host defense."
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"Recent studies have demonstrated that inhibiting USP15 prevents glutamate-induced oxidative stress and neuronal apoptosis by activating the NRF2/heme oxygenase 1 (HO-1) signaling pathway in HT22 cells [141]."
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"USP15 can stabilize MDM2 and negatively regulate the protein level of p53, and inactivation of USP15 can induce tumor apoptosis and improve the antitumor T-cell response[14]."
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"Targeting USP15 can induce apoptosis in tumor cells while enhancing anti-tumor T-cell responses."
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"In addition, apoptosis induction and proliferation inhibition can be caused by downregulation of USP15 expression."
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"Under these standard T cell differentiation conditions, USP15 deficient and wild-type T cells were similar in differentiation and proliferation, although the USP15 deficient T cells had moderately enhanced apoptosis compared to wild-type T cells (XREF_SUPPLEMENTARY)."
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"It was shown that when the XIAP gene was expressed in rat neonatal cardiomyocytes, it attenuated apoptosis induced by protein kinase C inhibition, hypoxia/ischemia, or isoproterenol stimulation.Ubiquitin-specific protease 15 (USP15), a member of cysteine protease deubiquitinases."
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"USP15 promotes the apoptosis of degenerative nucleus pulposus cells by suppressing the PI3K and AKT signalling pathway."
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"Crucially, ectopic expression of either p53 R175H or USP15 promoted p53 triggered apoptosis in human cervical cancer cells."
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