Mitochondria as the central control point of apoptosis (Q33994978)

30 July 2017

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title

Mitochondria as the central control point of apoptosis (English)

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30 July 2017

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Desagher S

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30 July 2017

Martinou JC

series ordinal

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30 July 2017

publication date

1 September 2000

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30 July 2017

published in

Trends in Cell Biology

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30 July 2017

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30 July 2017

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30 July 2017

page(s)

369-377

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Cell Death in Development

30 July 2017

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Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death

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The coordinate release of cytochrome c during apoptosis is rapid, complete and kinetically invariant

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Mitochondrial control of apoptosis

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The central executioner of apoptosis: multiple connections between protease activation and mitochondria in Fas/APO-1/CD95- and ceramide-induced apoptosis

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Distinct stages of cytochrome c release from mitochondria: evidence for a feedback amplification loop linking caspase activation to mitochondrial dysfunction in genotoxic stress induced apoptosis

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7 January 2021

Conversion of Bcl-2 to a Bax-like death effector by caspases

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7 January 2021

X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death

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Bcl-2 family proteins as ion-channels

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Ion channel activity of the BH3 only Bcl-2 family member, BID.

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Comparison of the ion channel characteristics of proapoptotic BAX and antiapoptotic BCL-2.

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Inhibition of Bax channel-forming activity by Bcl-2

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The Destabilization of Lipid Membranes Induced by the C-terminal Fragment of Caspase 8-cleaved Bid Is Inhibited by the N-terminal Fragment

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7 January 2021

Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations

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Identifiers

DOI

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30 July 2017

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