IndraLab

Statements

USP13 activates MCL1. 16 / 16
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"Taken together, our results indicated that pharmacological inhibition of USP13 by spautin-1 reduced MCL1 protein abundance and increased tumor cell sensitivity to ABT-263."
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"The deubiquitinase (DUB) USP13 promotes Mcl-1 stabilisation in cervical cancer."
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"We subsequently investigated the impact of USP13 mediated MCL1 stabilization on tumor malignancy."
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"Conversely, overexpression of WT USP13, but not the USP13 mutant, enhanced the half-life of Mcl-1 to ~ 300min."
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"Our data shows that USP13 and Mcl-1 protein expression correlates, suggesting that USP13 mediated Mcl-1 stabilisation is clinically relevant."
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"As a complimentary approach, we lentivirally expressed ectopic USP13 into OVCAR5, PC9 and NCI-H2170 cells, whose endogenous USP13 levels were relatively low, and found that overexpression of USP13 increased MCL1 protein, but not mRNA, abundance."
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"These data demonstrate that USP13 promotes the stability of Mcl-1 in HPV+ cervical cancer cells by protecting it from proteasomal degradation."
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"First, USP13 promoted MCL1 protein stability in multiple lung and ovarian cancer cell models."
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"In lung infection, USP13 are aberrantly expressed, inhibition of USP13 reduces the abundance of anti-apoptotic protein MCL1 in the lung [42]."
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"USP13 promotes MCL1 protein stability."
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"USP13 promotes Mcl-1 stability."
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"Finally, USP13 inhibition reduced MCL1 protein abundance and thereby increased tumor cell sensitivity to BH3 mimetic inhibitor ABT-263."
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"Conversely, exogenous USP13 overexpression evidently prolonged the half-life of endogenous MCL1 in NCI-H2170 and PC9 cells."
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"We concluded that USP13 promoted MCL1 stability at the post transcriptional level in lung and ovarian cancer cells."
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"USP13 knockdown by siRNA markedly reduced the half-life of MCL1 in TOV-21G and SW-1573 cells."
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"We further report that genetic or pharmacological inhibition of USP13 considerably reduces MCL1 protein abundance and significantly increases tumor cell sensitivity to BH3 mimetic inhibitors targeting BCL-2 and BCL-XL."
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