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USP9X activates cell death. 9 / 11
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"We found that inactivation of PRKAA2/USP9X showed little effect in normal condition, and slightly enhanced cell death in the absence of glucose (Figure 14)."
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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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"In this study, we revealed a molecular mechanism by which USP9X induces cell death."
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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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"Usp9X knock-down causes MPNST cell death with variable caspase activation and features of apoptosis."
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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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"Indeed, we observed that Mtb infection in FAF media significantly increased the cell death both in WT and ΔMMGT1 THP-1 macrophages, but with a much more pronounced effect in the latter cells (Fig. 4E)."
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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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"Because it has been demonstrated that ASK1 mediates oxidative stress-induced cell death through the activation of JNK and p38 pathways ( Noguchi et al., 2008; Tobiume et al., 2001 ), we examined the i[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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