The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
Bax-Dependent Caspase-3 Activation Is a Key Determinant in p53-Induced Apoptosis in Neurons
Open accessAbstract
p53 is a pivotal molecule regulating the death of neurons both after acute injury and during development. The molecular mechanisms by which p53 induces apoptosis in neuronal cells, however, are not well understood. We have shown previously that adenovirus-mediated p53 gene delivery to neurons was sufficient to induce apoptosis. In the present study we have examined the molecular mechanism by which p53 evokes neuronal cell death. Adenovirus-mediated delivery of p53 to cerebellar granule neurons resulted in caspase-3 (CPP32) activation followed by terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) staining and loss of viability as determined by an MTT survival assay. To determine whether Bax is essential for caspase-3 activation, p53 was expressed in Bax-deficient cells. Bax null neurons did not exhibit caspase-3 activation in response to p53 and were protected from apoptosis. To determine whether Bax-dependent caspase-3 activation was required in p53-mediated neuronal cell death, caspase-3-deficient neurons were examined. Our results indicate that caspase-3-deficient neurons exhibit a remarkable delay in apoptosis and a dramatic decrease in TUNEL-positive cells. These studies demonstrate that p53-induced cell death in postmitotic neurons involves a Bax-dependent caspase-3 activation, suggesting that these molecules are important determinants in neuronal cell death after injury.
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Cites
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Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
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Tumor suppressor p53 is a direct transcriptional activator of the human bax gene
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A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD
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Cited by
Blum, D., Torch, S., Lambeng, N., Nissou, M.-F., Benabid, A.-L., Sadoul, R., & Verna, J.-M. (2001) · Progress in Neurobiology · doi:10.1016/s0301-0082(01)00003-x · Cited by 1,246
Kruman, I. I., Culmsee, C., Chan, S. L., Kruman, Y., Guo, Z., Penix, L., & Mattson, M. P. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-18-06920.2000 · Cited by 784
Mechanisms of Early Brain Injury after Subarachnoid Hemorrhage
Cahill, W. J., Calvert, J. H., & Zhang, J. H. (2006) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/sj.jcbfm.9600283 · Cited by 630
Role of AIF in caspase-dependent and caspase-independent cell death
Cregan, S. P., Dawson, V. L., & Slack, R. S. (2004) · Oncogene · doi:10.1038/sj.onc.1207517 · Cited by 517
Self-citationApoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death
Cregan, S. P., Fortin, A., MacLaurin, J. G., Callaghan, S. M., Cecconi, F., Yu, S.-W., Dawson, T. M., Dawson, V. L., Park, D. S., Kroemer, G., et al. (2002) · The Journal of Cell Biology · doi:10.1083/jcb.200202130 · Cited by 477
Self-citation
Metadata
- Authors
- Cregan, S. P., MacLaurin, J. G., Craig, C. G., Robertson, G. S., Nicholson, D. W., Park, D. S., & Slack, R. S.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1999-09-15
- Volume
- 19
- Issue
- 18
- Pages
- 7860-7869
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1513688899
- Cited by
- 385
- References
- 70
- FWCI
- 9.03
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Bax-Dependent Caspase-3 Activation Is a Key Determinant in p53-Induced Apoptosis in Neurons. https://app.cochat.ai/papers/10.1523/jneurosci.19-18-07860.1999
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- Cregan, S. P., MacLaurin, J. G., Craig, C. G., Robertson, G. S., Nicholson, D. W., Park, D. S., & Slack, R. S. (1999). Bax-Dependent Caspase-3 Activation Is a Key Determinant in p53-Induced Apoptosis in Neurons. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.19-18-07860.1999
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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