Source:http://linkedlifedata.com/resource/pubmed/id/16215683
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2006-1-23
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pubmed:abstractText |
During development as well as in pathological situations, neurons that fail to find appropriate targets or neurotrophic factors undergo cell death. Using primary cortical neurons subjected to acute serum-deprivation (SD), we have examined caspases activation, mitochondrial dysfunction and cell death parameters. Among a panel of metabolic, signaling and caspases inhibitors only those able to interfere with caspase-2 like activity protect primary neurons against SD-induced cell death. In situ detection and subcellular fractionation demonstrate a very early activation of cytosolic caspase-2, which controls Bax cleavage, relocalization and mitochondrial membrane permeabilization (MMP). Both z-VDVAD-fmk and a siRNA specific for caspase-2 abolish Bax changes, mitochondrial membranes permeabilization, as well as cytochrome c release-dependent activation of caspase-9/caspase-3, nuclear alterations, phosphatidylserine exposure, neurites dismantling and neuronal death. Hence, caspase-2 is an early checkpoint for apoptosis initiation in primary neurons subjected to serum deprivation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cytochromes c,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1360-8185
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1243-59
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pubmed:meshHeading |
pubmed-meshheading:16215683-Animals,
pubmed-meshheading:16215683-Apoptosis,
pubmed-meshheading:16215683-Caspase 2,
pubmed-meshheading:16215683-Cell Survival,
pubmed-meshheading:16215683-Cells, Cultured,
pubmed-meshheading:16215683-Cytochromes c,
pubmed-meshheading:16215683-Enzyme Activation,
pubmed-meshheading:16215683-Enzyme Inhibitors,
pubmed-meshheading:16215683-Humans,
pubmed-meshheading:16215683-Mice,
pubmed-meshheading:16215683-Mitochondria,
pubmed-meshheading:16215683-Models, Biological,
pubmed-meshheading:16215683-Neurons,
pubmed-meshheading:16215683-Peptides,
pubmed-meshheading:16215683-Protein Transport,
pubmed-meshheading:16215683-RNA Interference,
pubmed-meshheading:16215683-Serum,
pubmed-meshheading:16215683-bcl-2-Associated X Protein
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pubmed:year |
2005
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pubmed:articleTitle |
Upstream control of apoptosis by caspase-2 in serum-deprived primary neurons.
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pubmed:affiliation |
Theraptosis Research Laboratory, Theraptosis S.A., Pasteur Biotop, Institut Pasteur, 25-28 Rue du Docteur Roux, 75015 Paris, France. dchauvier@theraptosis.com
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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