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• W2136885237 abstract "Axin, a negative regulator of Wnt signaling, participates in apoptosis, and Axin1 localizes to centrosomes and mitotic spindles, which requires Aurora kinase activity. In this study, Aurora inhibition of Axin1-expressing cells (L-Axin) produced polyploid cells, which died within 48 h posttreatment, whereas Axin2-expressing cells (L-Axin2) survived the same period. These cell death events showed apoptotic signs, such as chromatin condensation and increased sub-G1 populations, as well as cell membrane rupture. Further analysis showed that Aurora kinase inhibitor (AKI) treatment of L-Axin cells induced poly(ADP-ribose) polymerase (PARP) activation, which increased the poly(ADP-ribosyl)ation of cellular proteins and reduced cellular ATP content. PARP inhibition reduced a proportion of dead cells, suggesting PARP involvement in AKI-induced cell death. Also, AKI treatment of L-Axin cells induced mitochondrial apoptosis-inducing factor (AIF) release, but not mitochondrial cytochrome c release or caspase-3 activation. Knockdown of AIF attenuated AKI-induced cell death in L-Axin cells. Thus, our results suggest that Axin1 expression renders L929 cells sensitive to Aurora inhibition-induced cell death in a PARP- and AIF-dependent manner. J. Cell. Biochem. 112: 2392–2402, 2011. © 2011 Wiley-Liss, Inc." @default.
• W2136885237 created "2016-06-24" @default.
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• W2136885237 date "2011-08-18" @default.
• W2136885237 modified "2023-09-27" @default.
• W2136885237 title "Axin1 expression facilitates cell death induced by aurora kinase inhibition through PARP activation" @default.
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• W2136885237 doi "https://doi.org/10.1002/jcb.23162" @default.
• W2136885237 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21520248" @default.
• W2136885237 hasPublicationYear "2011" @default.
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