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• W2156770184 endingPage "1235" @default.
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• W2156770184 abstract "How cells die in the absence of oxygen (anoxia) is not understood. Here we report that cells deficient in Bax and Bak or caspase-9 do not undergo anoxia-induced cell death. However, the caspase-9 null cells do not survive reoxygenation due to the generation of mitochondrial reactive oxygen species. The individual loss of Bim, Bid, Puma, Noxa, Bad, caspase-2, or hypoxia-inducible factor 1beta, which are potential upstream regulators of Bax or Bak, did not prevent anoxia-induced cell death. Anoxia triggered the loss of the Mcl-1 protein upstream of Bax/Bak activation. Cells containing a mitochondrial DNA cytochrome b 4-base-pair deletion ([rho(-)] cells) and cells depleted of their entire mitochondrial DNA ([rho(0)] cells) are oxidative phosphorylation incompetent and displayed loss of the Mcl-1 protein under anoxia. [rho(0)] cells, in contrast to [rho(-)] cells, did not die under anoxia. However, [rho(0)] cells did undergo cell death in the presence of the Bad BH3 peptide, an inhibitor of Bcl-X(L)/Bcl-2 proteins. These results indicate that [rho(0)] cells survive under anoxia despite the loss of Mcl-1 protein due to residual prosurvival activity of the Bcl-X(L)/Bcl-2 proteins. Collectively, these results demonstrate that anoxia-induced cell death requires the loss of Mcl-1 protein and inhibition of the electron transport chain to negate Bcl-X(L)/Bcl-2 proteins." @default.
• W2156770184 created "2016-06-24" @default.
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• W2156770184 date "2007-02-01" @default.
• W2156770184 modified "2023-10-14" @default.
• W2156770184 title "Loss of Mcl-1 Protein and Inhibition of Electron Transport Chain Together Induce Anoxic Cell Death" @default.
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• W2156770184 doi "https://doi.org/10.1128/mcb.01535-06" @default.
• W2156770184 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1800715" @default.
• W2156770184 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17145774" @default.
• W2156770184 hasPublicationYear "2007" @default.
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