(Q24295878)

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Disruption of mitochondrial function during apoptosis is mediated by caspase cleavage of the p75 subunit of complex I of the electron transport chain

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Disruption of mitochondrial function during apoptosis is mediated by caspase cleavage of the p75 subunit of complex I of the electron transport chain (English)

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apoptotic process

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NADH:ubiquinone oxidoreductase core subunit S1

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GOA release 2020-03-11

reactive oxygen species metabolic process

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GOA release 2020-03-11

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inferred from title

Béatrice Bailly-Maitre

4

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Cristina Muñoz-Pinedo

2

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Douglas R. Green

object named as

Douglas R Green

9

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author name string

Jean-Ehrland Ricci

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Patrick Fitzgerald

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Guy A Perkins

5

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Nagendra Yadava

6

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Immo E Scheffler

7

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Mark H Ellisman

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publication date

11 June 2004

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117

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6

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773-86

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Redistribution of cytochrome c precedes the caspase-dependent formation of ultracondensed mitochondria, with a reduced inner membrane potential, in apoptotic monocytes

1 reference

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The nuclear encoded subunits of complex I from bovine heart mitochondria

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Human complex I deficiency: clinical spectrum and involvement of oxygen free radicals in the pathogenicity of the defect

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Fas-triggered phosphatidylserine exposure is modulated by intracellular ATP.

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Phosphatidylserine peroxidation/externalization during staurosporine-induced apoptosis in HL-60 cells

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Phosphatidylserine exposure in Fas type I cells is mitochondria-dependent

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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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Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis

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Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development

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A matter of life and death

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The NADH:ubiquinone oxidoreductase (complex I) of respiratory chains

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A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD

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

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A receptor for phosphatidylserine-specific clearance of apoptotic cells

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ABC1 promotes engulfment of apoptotic cells and transbilayer redistribution of phosphatidylserine

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Membrane blebbing during apoptosis results from caspase-mediated activation of ROCK I.

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Acinus is a caspase-3-activated protein required for apoptotic chromatin condensation

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The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore

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Caspase-independent cell death in T lymphocytes

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

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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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Many cuts to ruin: a comprehensive update of caspase substrates

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Mitochondrial functions during cell death, a complex (I–V) dilemma

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Internally quenched fluorescent peptide substrates disclose the subsite preferences of human caspases 1, 3, 6, 7 and 8

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The organization of NADH dehydrogenase polypeptides in the inner mitochondrial membrane

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Caspases induce cytochrome c release from mitochondria by activating cytosolic factors

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NADPH oxidase-dependent oxidation and externalization of phosphatidylserine during apoptosis in Me2SO-differentiated HL-60 cells. Role in phagocytic clearance

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Mitochondrial complex I inhibitor rotenone induces apoptosis through enhancing mitochondrial reactive oxygen species production

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Adenine nucleotide translocase-1, a component of the permeability transition pore, can dominantly induce apoptosis

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Caspase-mediated loss of mitochondrial function and generation of reactive oxygen species during apoptosis

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Isolation of intracellular membranes by means of sodium carbonate treatment: application to endoplasmic reticulum

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

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