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Failure of Bcl-2 to block cytochrome c redistribution during TRAIL-induced apoptosis

Date
2000
Abstract
Tumour necrosis factor (TNF)-related apoptosis inducing ligand (TRAIL) is a member of the TNF family of cytokines that promotes apoptosis and NF-kB activation. Here we show that recombinant hu-TRAIL initiates the activation of multiple caspases, the loss of mitochondrial transmembrane potential, the cleavage of BID and the redistribution of mitochondrial cytochrome c. However, whereas Bcl-2 efficiently blocked UV radiation-induced cytochrome c release and consequent apoptosis of CEM cells, it failed to do either in the context of TRAIL treatment. Thus, TRAIL engages a death pathway that is at least partially routed via the mitochondria, but in contrast with other stimuli that engage this pathway, TRAIL induced cytochrome c release is not regulated by Bcl-2.
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Description
peer-reviewed
Publisher
Elsevier
Citation
FEBS Letters;471/ 1/ pp 93-98
Collections
Glucksman Library
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2000_Keogh_TRAIL.pdf
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Keywords
apoptosis, Bcl-2, BID, Caspase, Cytochrome c, Tumor necrosis factor-related apoptosis-inducing ligand, Animal cell and molecular biology
ULRR Identifiers
https://hdl.handle.net/10344/2813
 https://doi.org/10.34961/9367
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Funding Information
Wellcome Trust
Sustainable Development Goals
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