Caspase-dependent and -independent death of camptothecin-treated embryonic cortical neurons. (Q48157353)

9 February 2018

title

Caspase-dependent and -independent death of camptothecin-treated embryonic cortical neurons. (English)

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9 February 2018

author name string

L Stefanis

1

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9 February 2018

D S Park

2

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9 February 2018

W J Friedman

3

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9 February 2018

L A Greene

4

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9 February 2018

language of work or name

English

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publication date

1 August 1999

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9 February 2018

published in

Journal of Neuroscience

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9 February 2018

volume

19

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9 February 2018

issue

15

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9 February 2018

page(s)

6235-6247

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9 February 2018

Mechanism of cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction.

cites work

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Induction of neuronal apoptosis by camptothecin, an inhibitor of DNA topoisomerase-I: evidence for cell cycle-independent toxicity

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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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Inhibitors of trypsin-like serine proteases inhibit processing of the caspase Nedd-2 and protect PC12 cells and sympathetic neurons from death evoked by withdrawal of trophic support

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Bcl-2 inhibits the mitochondrial release of an apoptogenic protease

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Beta-amyloid inhibition of MTT reduction is not mimicked by inhibitors of mitochondrial respiration.

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Multiple pathways of neuronal death induced by DNA-damaging agents, NGF deprivation, and oxidative stress

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The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease

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

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Effect of striatal cells on in vitro maturation of mesencephalic dopaminergic neurones grown in serum-free conditions

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Intracellular ATP levels determine cell death fate by apoptosis or necrosis.

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Caspases: intracellular signaling by proteolysis

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Neuroprotective actions of dipyridamole on cultured CNS neurons.

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Commitment and effector phases of the physiological cell death pathway elucidated with respect to Bcl-2 caspase, and cyclin-dependent kinase activities

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Nedd2 is required for apoptosis after trophic factor withdrawal, but not superoxide dismutase (SOD1) downregulation, in sympathetic neurons and PC12 cells

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Bax involvement in p53-mediated neuronal cell death

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Differential actions of neurotrophins in the locus coeruleus and basal forebrain

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The central executioners of apoptosis: caspases or mitochondria?

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12 December 2020

Mitochondria and apoptosis

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12 December 2020

Caspase-2 (Nedd-2) processing and death of trophic factor-deprived PC12 cells and sympathetic neurons occur independently of caspase-3 (CPP32)-like activity

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Blocking cytochrome c activity within intact neurons inhibits apoptosis.

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Inhibitors of cyclin-dependent kinases promote survival of post-mitotic neuronally differentiated PC12 cells and sympathetic neurons

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Characterization of the cellular reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT): subcellular localization, substrate dependence, and involvement of mitochondrial electron transport in MTT reduction

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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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12 December 2020

Identifiers

PubMed ID

10414953

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9 February 2018