ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Exogenous smac induces competence and permits caspase activation in sympathetic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
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- mRNA for N-Bak, a neuron-specific BH3-only splice isoform of Bak, escapes nonsense-mediated decay and is translationally repressed in the neurons.Cell death & disease · 2012Article
- Bax regulates production of superoxide in both apoptotic and nonapoptotic neurons: role of caspases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Features of programmed cell death in intact Xenopus oocytes and early embryos revealed by near-infrared fluorescence and real-time monitoring.Cell death and differentiation · 2010Article
- Review
- Differential regulation of Smac/DIABLO and Hsp-70 during brain maturation.Neuromolecular medicine · 2007Article
- Reduced Apaf-1 levels in cardiomyocytes engage strict regulation of apoptosis by endogenous XIAP.The Journal of cell biology · 2005Article
- Cell differentiation: reciprocal regulation of Apaf-1 and the inhibitor of apoptosis proteins.The Journal of cell biology · 2004Review
- Decreased apoptosome activity with neuronal differentiation sets the threshold for strict IAP regulation of apoptosis.The Journal of cell biology · 2004Article
- Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology.The Journal of experimental medicine · 2004Article
- The kinder side of killer proteases: caspase activation contributes to neuroprotection and CNS remodeling.Apoptosis : an international journal on programmed cell death · 2004Review
- Induction of apoptosis in starfish eggs requires spontaneous inactivation of MAPK (extracellular signal-regulated kinase) followed by activation of p38MAPK.Molecular biology of the cell · 2004Article
- GDNF-deprived sympathetic neurons die via a novel nonmitochondrial pathway.The Journal of cell biology · 2003Article
- Critical function of endogenous XIAP in regulating caspase activation during sympathetic neuronal apoptosis.The Journal of cell biology · 2003Article
- Dmp53 protects the Drosophila retina during a developmentally regulated DNA damage response.The EMBO journal · 2003Article
- Real-time single cell analysis of Smac/DIABLO release during apoptosis.The Journal of cell biology · 2003Article
- Gap junctions mediate bystander cell death in developing retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Studies on neuronal apoptosis in primary forebrain cultures: neuroprotective/anti-apoptotic action of NR2B NMDA antagonists.Neurotoxicity research · 2003Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sympathetic neuronal apoptosis after nerve growth factor (NGF) deprivation requires the activation of two events: a protein synthesis-dependent, Bax-dependent release of mitochondrial cytochrome c and a protein synthesis-independent, Bax-independent development of competence. Unlike in most cells, cytosolic cytochrome c is not sufficient to induce cell death in NGF-maintained sympathetic neurons but can do so in neurons that have developed competence. We report that cytosolic cytochrome c-induced apoptosis in competent sympathetic neurons is completely dependent on caspase-9. In addition, the neuroprotective agents KCl and chlorophenylthio-cAMP are potent inhibitors of the development-of-competence pathway in NGF-deprived sympathetic neurons. We also find that the development of competence is reversible. Readdition of NGF reverses competence, and neurons can regain their resistance to cytosolic cytochrome c. Importantly, we examined the mechanism of development of competence and report that the inability of cytochrome c to activate caspases in NGF-maintained sympathetic neurons can be overcome with exogenous Smac that inhibits the inhibitor of apoptosis (IAP) family of proteins. Microinjection of cytochrome c and Smac, but neither alone, induces rapid cell death in NGF-maintained neurons. These data suggest that development of competence may be the result of the loss of the function of one or more members of the IAP family of caspase inhibitors that is needed before cytochrome c can activate caspases and induce cell death in neurons.
Indexed as
Identifiers
12223555PMC6758081W2101985096What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.