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• W2974887893 abstract "TNF α /CHX-induced apoptosis is dependent on caspase-8 activation and regulated by Bcl-2. However, the specific participants and precise mechanisms underlying this apoptotic pathway are poorly understood. The proapoptotic proteins Bak and Bax—members of the Bcl-2 family—are essential for the functioning of the mitochondrial apoptotic pathway. In this study, we used the CRISPR/Cas9 system to knockout Bak in the human SH-SY5Y cell line and determined the effects of this knockout on TNF α /CHX-induced apoptosis. Our data showed that overexpression of Bcl-2 dramatically prevented TNF α /CHX-induced apoptosis, and then pro-apoptotic protein Bak was downregulated and became more resistant to TNF α /CHX-induced apoptosis, because both TNF α /CHX-induced PARP cleavage and caspase activation were blocked in BAK−/− cells or using specific siRNA, whereas Bax was dispensable in TNF α /CHX-induced apoptosis, as evidenced using specific siRNA. Bax translocated from the cytosol into the mitochondria in response to TNF α /CHX, and CRISPR/Cas9 knockout of Bak significantly decreased this translocation. These results indicate that TNF α /CHX-induced apoptosis does not occur in Bak−/− cells, suggesting that TNF α /CHX-induced apoptosis is Bak-dependent but Bax-independent." @default.
• W2974887893 created "2019-09-26" @default.
• W2974887893 creator A5033994290 @default.
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• W2974887893 date "2019-09-17" @default.
• W2974887893 modified "2023-10-17" @default.
• W2974887893 title "CRISPR/Cas9 Knockout of Bak Mediates Bax Translocation to Mitochondria in response to TNF<i>α</i>/CHX-induced Apoptosis" @default.
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• W2974887893 doi "https://doi.org/10.1155/2019/9071297" @default.
• W2974887893 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6766168" @default.
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