(Q28217828)

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Anne Druilhe

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Teresa Fernandes-Alnemri

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Emad S Alnemri

Journal of Biological Chemistry

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language of work or name

English

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publication date

19 April 2002

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published in

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volume

277

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issue

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page(s)

13430-7

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cites work

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A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain

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Membrane oligomerization and cleavage activates the caspase-8 (FLICE/MACHalpha1) death signal

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Molecular ordering of the Fas-apoptotic pathway: the Fas/APO-1 protease Mch5 is a CrmA-inhibitable protease that activates multiple Ced-3/ICE-like cysteine proteases

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Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked

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Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade

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Molecular determinants of the caspase-promoting activity of Smac/DIABLO and its role in the death receptor pathway

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Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins

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Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition

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Identification and Molecular Cloning of Two Novel Receptors for the Cytotoxic Ligand TRAIL

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Caspase-2 is localized at the Golgi complex and cleaves golgin-160 during apoptosis

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Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas death

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Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosis

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Two distinct pathways leading to nuclear apoptosis

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Bcl-2 family: life-or-death switch

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Bcl-xL Regulates the Membrane Potential and Volume Homeostasis of Mitochondria

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The release of cytochrome c from mitochondria during apoptosis of NGF-deprived sympathetic neurons is a reversible event

21 January 2018

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Bax-induced cytochrome C release from mitochondria is independent of the permeability transition pore but highly dependent on Mg2+ ions

21 January 2018

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Bax directly induces release of cytochrome c from isolated mitochondria

21 January 2018

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Bax-induced caspase activation and apoptosis via cytochrome c release from mitochondria is inhibitable by Bcl-xL.

21 January 2018

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Bcl-x(L) forms an ion channel in synthetic lipid membranes.

21 January 2018

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Inhibition of Bax channel-forming activity by Bcl-2

21 January 2018

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

21 January 2018

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Recent progress on regulation of the mitochondrial permeability transition pore; a cyclosporin-sensitive pore in the inner mitochondrial membrane

21 January 2018

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Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC

21 January 2018

1 reference

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Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity

21 January 2018

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FLICE Induced Apoptosis in a Cell-free System

21 January 2018

1 reference

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21 January 2018

Identifiers

DOI

10.1074/JBC.M108029200

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

11832478

1 reference

Consolidated OpenCitations Corpus – April 2017