(Q43700527)

English

Mitochondrial cytochrome c release is caspase-dependent and does not involve mitochondrial permeability transition in didemnin B-induced apoptosis

scientific article published in July 2001

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scholarly article

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

Mitochondrial cytochrome c release is caspase-dependent and does not involve mitochondrial permeability transition in didemnin B-induced apoptosis (English)

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

author name string

Grubb DR

1

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

Ly JD

2

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

Vaillant F

3

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

Johnson KL

4

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

Lawen A

5

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

language of work or name

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publication date

1 July 2001

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

20

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

30

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

4085-4094

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

https://scigraph.springernature.com/pub.10.1038/sj.onc.1204545

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Bcl-2 and Bax regulate the channel activity of the mitochondrial adenine nucleotide translocator

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

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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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Didemnin binds to the protein palmitoyl thioesterase responsible for infantile neuronal ceroid lipofuscinosis

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Mitochondria as the central control point of apoptosis

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mtDNA-depleted U937 cells are sensitive to TNF and Fas-mediated cytotoxicity

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

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A rapid and simple method for the isolation of apoptotic DNA fragments.

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From calcium signaling to cell death: two conformations for the mitochondrial permeability transition pore. Switching from low- to high-conductance state

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Bcl-2 blocks apoptosis in cells lacking mitochondrial DNA.

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Rapamycin inhibits didemnin B-induced apoptosis in human HL-60 cells: evidence for the possible involvement of FK506-binding protein 25

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

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Release of caspase-9 from mitochondria during neuronal apoptosis and cerebral ischemia

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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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Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c

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Mitochondrial permeability transition is a central coordinating event of apoptosis

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The antiproliferative agent didemnin B uncompetitively inhibits palmitoyl protein thioesterase

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Matrix detachment induces caspase-dependent cytochrome c release from mitochondria: inhibition by PKB/Akt but not Raf signalling

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BAX-dependent transport of cytochrome c reconstituted in pure liposomes

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JC-1, but not DiOC6(3) or rhodamine 123, is a reliable fluorescent probe to assess delta psi changes in intact cells: implications for studies on mitochondrial functionality during apoptosis

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Commitment to apoptosis by GD3 ganglioside depends on opening of the mitochondrial permeability transition pore.

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Ordering the cytochrome c-initiated caspase cascade: hierarchical activation of caspases-2, -3, -6, -7, -8, and -10 in a caspase-9-dependent manner

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Molecular characterization of mitochondrial apoptosis-inducing factor

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Human cell mutants with very low mitochondrial DNA copy number (rho d).

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Didemnins A and B. Effectiveness against cutaneous herpes simplex virus in mice

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

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Sequential reduction of mitochondrial transmembrane potential and generation of reactive oxygen species in early programmed cell death

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Inhibitors of permeability transition interfere with the disruption of the mitochondrial transmembrane potential during apoptosis.

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Reduction in mitochondrial potential constitutes an early irreversible step of programmed lymphocyte death in vivo.

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

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Apoptosis, in human monocytic THP.1 cells, results in the release of cytochrome c from mitochondria prior to their ultracondensation, formation of outer membrane discontinuities and reduction in inner membrane potential

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Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3

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The structure of bongkrekic acid

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Didemnin B induces cell death by apoptosis: the fastest induction of apoptosis ever described

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Bid-induced cytochrome c release is mediated by a pathway independent of mitochondrial permeability transition pore and Bax.

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Identifiers

10.1038/SJ.ONC.1204545

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

Dimensions Publication ID

0 references

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

26 November 2017

ResearchGate publication ID

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