And all of a sudden it's over: mitochondrial outer-membrane permeabilization in apoptosis (Q34648801)

3 August 2017

title

And all of a sudden it's over: mitochondrial outer-membrane permeabilization in apoptosis (English)

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3 August 2017

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Douglas R Green

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author name string

Nigel J Waterhouse

series ordinal

1

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3 August 2017

Jean-Ehrland Ricci

series ordinal

2

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3 August 2017

publication date

1 February 2002

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3 August 2017

language of work or name

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3 August 2017

volume

84

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3 August 2017

issue

2-3

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3 August 2017

page(s)

113-121

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publication type of scholarly work

3 August 2017

review article

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Pro-caspase-3 is a major physiologic target of caspase-8.

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Cleavage of CPP32 by granzyme B represents a critical role for granzyme B in the induction of target cell DNA fragmentation

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The cytotoxic cell protease granzyme B initiates apoptosis in a cell-free system by proteolytic processing and activation of the ICE/CED-3 family protease, CPP32, via a novel two-step mechanism.

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FLICE is activated by association with the CD95 death-inducing signaling complex (DISC).

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Isolation and analysis of components of CD95 (APO-1/Fas) death-inducing signaling complex

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Defective cytochrome c-dependent caspase activation in ovarian cancer cell lines due to diminished or absent apoptotic protease activating factor-1 activity

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An APAF-1.cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9

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Cytochrome c and dATP-mediated oligomerization of Apaf-1 is a prerequisite for procaspase-9 activation

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Granzyme B-mediated apoptosis proceeds predominantly through a Bcl-2-inhibitable mitochondrial pathway

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Initiation of apoptosis by granzyme B requires direct cleavage of bid, but not direct granzyme B-mediated caspase activation.

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Anti-apoptotic oncogenes prevent caspase-dependent and independent commitment for cell death

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Bcl-2-independent Bcr-Abl-mediated resistance to apoptosis: protection is correlated with up regulation of Bcl-xL.

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In vivo veritas: Bcl-2 and Bcl-X(L)mediate tumor cell resistance to chemotherapy

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Inhibition of Ced-3/ICE-related proteases does not prevent cell death induced by oncogenes, DNA damage, or the Bcl-2 homologue Bak

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

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Evidence of a novel event during neuronal death: development of competence-to-die in response to cytoplasmic cytochrome c

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Protein import into mitochondria

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The Tom and Tim machine

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Mmicular mechanisms of cytochrome c biogenesis: three distinct systems

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7 January 2021

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

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Apoptosis induced by microinjection of cytochrome c is caspase-dependent and is inhibited by Bcl-2.

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Blocking cytochrome c activity within intact neurons inhibits apoptosis.

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

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DIABLO promotes apoptosis by removing MIHA/XIAP from processed caspase 9

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The Ca2+-induced membrane transition in mitochondria

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Mitochondria and cell death. Mechanistic aspects and methodological issues

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Regulation of the permeability transition pore, a voltage-dependent mitochondrial channel inhibited by cyclosporin A

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Mitochondrial control of nuclear apoptosis.

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The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis

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7 January 2021

Bcl-2 inhibits the mitochondrial release of an apoptogenic protease

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7 January 2021

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

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7 January 2021

Mitochondrial depolarization accompanies cytochrome c release during apoptosis in PC6 cells

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7 January 2021

Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process

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7 January 2021

Electrical coupling and plasticity of the mitochondrial network

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Cyclophilin-D binds strongly to complexes of the voltage-dependent anion channel and the adenine nucleotide translocase to form the permeability transition pore

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The mitochondrial permeability transition: its molecular mechanism and role in reperfusion injury

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The Permeability Transition Pore Complex: A Target for Apoptosis Regulation by Caspases and Bcl-2–related Proteins

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7 January 2021

Bax-induced Cytochrome C Release from Mitochondria Is Independent of the Permeability Transition Pore but Highly Dependent on Mg2+ Ions

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7 January 2021

Collapse of the inner mitochondrial transmembrane potential is not required for apoptosis of HL60 cells.

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7 January 2021

Lonidamine triggers apoptosis via a direct, Bcl-2-inhibited effect on the mitochondrial permeability transition pore

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7 January 2021

The protonophore CCCP induces mitochondrial permeability transition without cytochrome c release in human osteosarcoma cells

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7 January 2021

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

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7 January 2021

Bcl-xL prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange

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7 January 2021

Bcl-xL promotes the open configuration of the voltage-dependent anion channel and metabolite passage through the outer mitochondrial membrane

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7 January 2021

In the absence of extrinsic signals, nutrient utilization by lymphocytes is insufficient to maintain either cell size or viability

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7 January 2021

The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

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7 January 2021

Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

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7 January 2021

The conserved N-terminal BH4 domain of Bcl-2 homologues is essential for inhibition of apoptosis and interaction with CED-4

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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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7 January 2021

Solution structure of BID, an intracellular amplifier of apoptotic signaling

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7 January 2021

Solution structure of the proapoptotic molecule BID: a structural basis for apoptotic agonists and antagonists

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7 January 2021

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

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7 January 2021

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

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7 January 2021

Channel formation by antiapoptotic protein Bcl-2.

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7 January 2021

Inhibition of Bax channel-forming activity by Bcl-2

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7 January 2021

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

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7 January 2021

Changes in intramitochondrial and cytosolic pH: early events that modulate caspase activation during apoptosis

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7 January 2021

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

Characterization of tBid-induced cytochrome c release from mitochondria and liposomes

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7 January 2021

Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c.

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7 January 2021

Pro-apoptotic cleavage products of Bcl-xL form cytochrome c-conducting pores in pure lipid membranes

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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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7 January 2021

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

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7 January 2021

Electrophysiological study of a novel large pore formed by Bax and the voltage-dependent anion channel that is permeable to cytochrome c.

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7 January 2021

Heat-shock protein 70 inhibits apoptosis by preventing recruitment of procaspase-9 to the Apaf-1 apoptosome

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7 January 2021

A novel enhancer of the Apaf1 apoptosome involved in cytochrome c-dependent caspase activation and apoptosis

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7 January 2021

Inactivation of the apoptosis effector Apaf-1 in malignant melanoma

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7 January 2021

Preservation of mitochondrial structure and function after Bid- or Bax-mediated cytochrome c release

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7 January 2021

Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization.

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7 January 2021

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

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7 January 2021

Bax directly induces release of cytochrome c from isolated mitochondria

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7 January 2021

A reversible component of mitochondrial respiratory dysfunction in apoptosis can be rescued by exogenous cytochrome c.

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7 January 2021

The (Holey) study of mitochondria in apoptosis

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7 January 2021

10.1016/S0300-9084(02)01379-2

Identifiers

DOI

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3 August 2017

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