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

Sinead A. Keogh; Henning Walczak; Lisa Bouchier-Hayes; Seamus J. Martin

doi:10.1016/S0014-5793(00)01375-2

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

Sinead A. Keogh, Henning Walczak, Lisa Bouchier-Hayes, Seamus J. Martin

Research output: Contribution to journal › Article › peer-review

Abstract

Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family of cytokines that promotes apoptosis and NF-κB 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. Copyright (C) 2000 Federation of European Biochemical Societies.

Original language	English
Pages (from-to)	93-98
Number of pages	6
Journal	FEBS Letters
Volume	471
Issue number	1
DOIs	https://doi.org/10.1016/S0014-5793(00)01375-2
Publication status	Published - 7 Apr 2000
Externally published	Yes

Keywords

Apoptosis
Bcl-2
BID
Caspase
Cytochrome c
Tumor necrosis factor-related apoptosis-inducing ligand

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S0014-5793(00)01375-2

Cite this

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title = "Failure of Bcl-2 to block cytochrome c redistribution during TRAIL-induced apoptosis",

abstract = "Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family of cytokines that promotes apoptosis and NF-κB 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. Copyright (C) 2000 Federation of European Biochemical Societies.",

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T1 - Failure of Bcl-2 to block cytochrome c redistribution during TRAIL-induced apoptosis

AU - Keogh, Sinead A.

AU - Walczak, Henning

AU - Bouchier-Hayes, Lisa

AU - Martin, Seamus J.

PY - 2000/4/7

Y1 - 2000/4/7

N2 - Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family of cytokines that promotes apoptosis and NF-κB 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. Copyright (C) 2000 Federation of European Biochemical Societies.

AB - Tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family of cytokines that promotes apoptosis and NF-κB 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. Copyright (C) 2000 Federation of European Biochemical Societies.

KW - Apoptosis

KW - Bcl-2

KW - BID

KW - Caspase

KW - Cytochrome c

KW - Tumor necrosis factor-related apoptosis-inducing ligand

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U2 - 10.1016/S0014-5793(00)01375-2

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SN - 0014-5793

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ER -

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

Abstract

Keywords

UN SDGs

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