IndraLab

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USP9X inhibits cell death. 13 / 13
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"Given that ATF3 and ATF4 are downstream regulators of the ER-stress response and are capable of activating Noxa , we hypothesized that cell death induced by Usp9X inhibition may in part be mediated through an ER stress response."
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"Usp9X inhibition induces cell death with features of apoptosis and loss of membrane potential in MPNST cell lines ."
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"Moreover, pharmacological inhibition of USP9X potently induced cell death in oral cancer cells through rapid degradation of Mcl-1 [37]."
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"USP9X knockdown enhances cell death caused by the Bcl-2 homology 3 mimetic ABT-737 (11)."
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"Indeed, knockdown of Usp9X increased mitotic cell death in Mcl1 -/- cells to a similar extent as in WT MEFs, thus indicating independence of MCL1 (Fig XREF_FIG A and B)."
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"Interestingly, different from Peterson 's finding that USP9X is an oncogene in B-cell malignancies [XREF_BIBR], we found that knockdown of USP9X did not induce cell death of T-ALL cells, indicating that the role of USP9X is cell type dependent."
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"Pharmacological inhibition of USP9X potently induced cell death in OSCC cells in vitro and in vivo."
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"However, taking this speculation aside, at the minimum, increased Noxa levels will facilitate release of BAK and BIM from Mcl-1, thereby driving BAX/BAK mediated intrinsic apoptosis.In seeking to identify others forms of cell death produced by Usp9X inhibition in MPNST cells, TEM analysis showed morphological features of paraptosis with extensive cytoplasmic vacuolization, swelling of ER and mitochondria and only minimal features of apoptosis ."
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"Moreover, USP9x silencing resulted in significantly increased cell death in BaF3 and p210 cells (XREF_SUPPLEMENTARY), suggesting that the ITC induced inhibition of USP9x can, at least partially, account for the reduced viability and increased cell death observed upon ITC treatment."
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"Our findings suggest that Usp9X and Mcl-1 are novel targets for the treatment of MPNSTs and that paraptosis, a caspase-independent type of regulated cell death, may play a role in MPNST cell death induced by Usp9X inhibition."
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"Furthermore, USP9X-deficient cells showed resistance to oxidative stress-induced cell death accompanied by reduced activation of JNK."
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"However, a few studies have suggested that USP9X has roles in hematological tumors.141 142 USP9X was found to inhibit cell death by inhibiting the ubiquitin degradation of myeloid cell leukemia-1 thus promoting disease progression."
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"To determine if caspase-dependent apoptosis is the main cell death pathway activated by Usp9X or Mcl-1 depletion, we tested the ability of ZVAD, a broad-spectrum caspase inhibitor, to inhibit Usp9X and Mcl-1 knock-down induced MPNST cell death."
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