IndraLab

Statements


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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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"Usp9X knock-down causes MPNST cell death with variable caspase activation and features of apoptosis."

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"Since centrosome dysregulation associated mitotic defects could result in genome instability and cell apoptosis XREF_BIBR XREF_BIBR XREF_BIBR, we examined whether USP9X promoted CEP131 stabilization plays a role in genome stability and cell death."

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"It is thus possible that USP9X promotes or prevents H 2 O 2 -triggered cell death by acting on different targets at varying levels of oxidative damage."

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"Thus, USP9X positively regulates ASK1 activity and ASK1 dependent cell death through the deubiquitination and stabilization of ASK1 [XREF_BIBR]."

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"Finally, the Usp9X pharmacological inhibitor WP1130 significantly reduced human MPNST growth and induced tumor cell death in an in vivo xenograft model."