ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Nuclear factor-(kappa)B modulates the p53 response in neurons exposed to DNA damage.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 108 citations in OpenAlex.
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- The Effect of Simvastatin on the Dynamics of NF-κB-Regulated Neurodegenerative and Neuroprotective Processes in the Acute Phase of Ischemic Stroke.Molecular neurobiology · 2023Article
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- Magnesium acetyltaurate prevents retinal damage and visual impairment in rats through suppression of NMDA-induced upregulation of NF-κB, p53 and AP-1 (c-Jun/c-Fos).Neural regeneration research · 2021Article
- The Preeclamptic Environment Promotes the Activation of Transcription Factor Kappa B by P53/RSK1 Complex in a HTR8/SVneo Trophoblastic Cell Line.International journal of molecular sciences · 2021Article
- Apoptotic cell death regulation in neurons.The FEBS journal · 2019Review
- Activating Mas receptor protects human pulmonary microvascular endothelial cells against LPS-induced apoptosis via the NF-kB p65/P53 feedback pathways.Journal of cellular physiology · 2019Article
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- Ubiquilin-2 drives NF-κB activity and cytosolic TDP-43 aggregation in neuronal cells.Molecular brain · 2015Article
- The Regulatory Machinery of Neurodegeneration in In Vitro Models of Amyotrophic Lateral Sclerosis.Cell reports · 2015Article
- Regulation of the VHL/HIF-1 pathway by DJ-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Neuroprotective and neurite outgrowth effects of maltol on retinal ganglion cells under oxidative stress.Molecular vision · 2014Article
- DJ-1 interacts with and regulates paraoxonase-2, an enzyme critical for neuronal survival in response to oxidative stress.PloS one · 2014Article
- MPT64 protein from Mycobacterium tuberculosis inhibits apoptosis of macrophages through NF-kB-miRNA21-Bcl-2 pathway.PloS one · 2014Article
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- Cathepsin L plays a role in quinolinic acid-induced NF-Κb activation and excitotoxicity in rat striatal neurons.PloS one · 2013Article
- Apoptosis induced by mammalian reovirus is beta interferon (IFN) independent and enhanced by IFN regulatory factor 3- and NF-κB-dependent expression of Noxa.Journal of virology · 2012Article
- The bad, the good, and the ugly about oxidative stress.Oxidative medicine and cellular longevity · 2012Review
- Deregulation of TDP-43 in amyotrophic lateral sclerosis triggers nuclear factor κB-mediated pathogenic pathways.The Journal of experimental medicine · 2011Article
- Parkin is transcriptionally regulated by ATF4: evidence for an interconnection between mitochondrial stress and ER stress.Cell death and differentiation · 2011Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that DNA damage-evoked death of primary cortical neurons occurs in a p53 and cyclin-dependent kinase-dependent (CDK) manner. The manner by which these signals modulate death is unclear. Nuclear factor-kappaB (NF-kappaB) is a group of transcription factors that potentially interact with these pathways. Presently, we show that NF-kappaB is activated shortly after induction of DNA damage in a manner independent of the classic IkappaB kinase (IKK) activation pathway, CDKs, ATM, and p53. Acute inhibition of NF-kappaB via expression of a stable IkappaB mutant, downregulation of the p65 NF-kappaB subunit by RNA interference (RNAi), or pharmacological NF-kappaB inhibitors significantly protected against DNA damage-induced neuronal death. NF-kappaB inhibition also reduced p53 transcripts and p53 activity as measured by the p53-inducible messages, Puma and Noxa, implicating the p53 tumor suppressor in the mechanism of NF-kappaB-mediated neuronal death. Importantly, p53 expression still induces death in the presence of NF-kappaB inhibition, indicating that p53 acts downstream of NF-kappaB. Interestingly, neurons cultured from p65 or p50 NF-kappaB-deficient mice were not resistant to death and did not show diminished p53 activity, suggesting compensatory processes attributable to germline deficiencies, which allow p53 activation still to occur. In contrast to acute NF-kappaB inhibition, prolonged NF-kappaB inhibition caused neuronal death in the absence of DNA damage. These results uniquely define a signaling paradigm by which NF-kappaB serves both an acute p53-dependent pro-apoptotic function in the presence of DNA damage and an anti-apoptotic function in untreated normal neurons.
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