ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Apoptotic actions of p53 require transcriptional activation of PUMA and do not involve a direct mitochondrial/cytoplasmic site of action in postnatal cortical neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 61 citations in OpenAlex.
- MDM2 inhibitors-mediated disruption of mitochondrial metabolism: A novel therapeutic strategy for retinoblastoma.Frontiers in oncology · 2022Review
- SAHA is neuroprotective in in vitro and in situ models of retinitis pigmentosa.Molecular vision · 2021Article
- Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins.Cell death and differentiation · 2021Review
- Down-Regulation of miR-23a-3p Mediates Irradiation-Induced Neuronal Apoptosis.International journal of molecular sciences · 2020Article
- Article
- NFBD1/MDC1 participates in the regulation of proliferation and apoptosis in human laryngeal squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018Article
- Glioma targeting peptide in combination with the P53 C terminus inhibits glioma cell proliferation in vitro.Cytotechnology · 2018Article
- Cofilin-mediated Neuronal Apoptosis via p53 Translocation and PLD1 Regulation.Scientific reports · 2017Article
- NDRG2 promotes adriamycin sensitivity through a Bad/p53 complex at the mitochondria in breast cancer.Oncotarget · 2017Article
- Post-traumatic administration of the p53 inactivator pifithrin-α oxygen analogue reduces hippocampal neuronal loss and improves cognitive deficits after experimental traumatic brain injury.Neurobiology of disease · 2016Article
- Multiple faces of dynamin-related protein 1 and its role in Alzheimer's disease pathogenesis.Biochimica et biophysica acta · 2016Review
- p53 and mitochondrial function in neurons.Biochimica et biophysica acta · 2014Review
- DAPK1-p53 interaction converges necrotic and apoptotic pathways of ischemic neuronal death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- MS-275, a class I histone deacetylase inhibitor, protects the p53-deficient mouse against ischemic injury.Journal of neurochemistry · 2014Article
- Bax interacting factor-1 promotes survival and mitochondrial elongation in neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Novel protective effects of histone deacetylase inhibition on stroke and white matter ischemic injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2013Review
- Specific acetylation of p53 by HDAC inhibition prevents DNA damage-induced apoptosis in neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Olesoxime protects embryonic cortical neurons from camptothecin intoxication by a mechanism distinct from BDNF.British journal of pharmacology · 2013Article
- Declines in Drp1 and parkin expression underlie DNA damage-induced changes in mitochondrial length and neuronal death.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies in non-neuronal cells have shown that the tumor suppressor p53 can promote cell death through a transcription-independent mechanism involving its direct action with a subset of Bcl-2 family member proteins in the cytosol and at the mitochondria. In cultured cortical neurons, however, we could not find evidence supporting a significant contribution of the cytosolic/mitochondrial p53 pathway, and available evidence instead corroborated the requirement for the transcriptional activity of p53. When directly targeted to the cytosol/mitochondria, wild-type p53 lost its apoptosis-inducing activity in neurons but not in non-neuronal cells. The N-terminal p53 fragment (transactivation and proline-rich domains), which induces apoptosis in non-neuronal cells via the cytosolic/mitochondrial pathway, displayed no apoptogenic activity in neurons. In neuronal apoptosis induced by camptothecin or an MDM2 (murine double minute 2) inhibitor, nutlin-3, endogenous p53 protein did not accumulate in the cytosol/mitochondria, and transcriptional inhibition after p53 induction effectively blocked cell death. In addition, overexpression of a dominant-negative form of p53 (R273H) completely suppressed induction of proapoptotic p53 target genes and cell death. PUMA (p53-upregulated modulator of apoptosis) was one such gene induced by camptothecin, and its overexpression was sufficient to induce Bax (Bcl-2-associated X protein)-dependent neuronal death, whereas Noxa was not apoptogenic. These results collectively demonstrate that, in contrast to non-neuronal cells, the apoptotic activity of p53 in postnatal cortical neurons does not rely on its direct action at the cytosol/mitochondria but is exclusively mediated through its transcription-dependent functions. The uniqueness of p53-mediated apoptotic signaling in postnatal cortical neurons was further illustrated by the dispensable function of the proline-rich domain of p53.
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