The DOI matches its Crossref record; 34 of the 35 references it cites were found in a registry or an index.
Forebrain-Specific Neuronal Inhibition of Nuclear Factor-κB Activity Leads to Loss of Neuroprotection
Open accessAbstract
The transcription factor Rel/nuclear factor (NF)-κB is known for its fundamental role in regulating immune and inflammatory responses. In the brain, constitutive NF-κB activity has been detected exclusively in neurons, and a large diversity of stimuli have been reported to induce NF-κB activity. Yet the function of this transcription factor in the nervous system remains unclear, and its role in neuroprotection or neurodegeneration is open to debate. Recently it was suggested that κB-driven gene expression in neurons is controlled by Sp1-like factors. To clarify such controversy, we have characterized here a novel mouse model in which the entire NF-κB-dependent transcriptional response is abolished in the forebrain. Calcium-calmodulin-dependent kinase II α promoter-driven tetracycline transactivator was used for regulated expression of a transdominant negative mutant of inhibitor κBα (super-repressor) together with a green fluorescent protein tracer. Inhibition of expression of a κB-dependent lacZ transgene was shown in triple transgenic mice, which correlated with the loss of κB-specific DNA binding. In transgenic organotypic hippocampal slice cultures, expression of the super-repressor led to strong cell death after neurotoxic insults. These data demonstrate for the first time that neuron-restricted ablation of NF-κB-driven gene expression increases neurodegeneration. This might lead to the path for new treatments of neurodegenerative diseases.
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“Furthermore, suppression of neuronal NF‐kB in vivo renders neurons more susceptible to kainic acid‐induced neurotoxicity (Fridmacher et al, 2003).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Fridmacher et al, 2003
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Self-citationNF-κB in neuronal plasticity and neurodegenerative disorders
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Metadata
- Authors
- Fridmacher, V., Kaltschmidt, B., Goudeau, B., Ndiaye, D., Rossi, F. M., Pfeiffer, J., Kaltschmidt, C., Israël, A., & Mémet, S.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2003-10-15
- Volume
- 23
- Issue
- 28
- Pages
- 9403-9408
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6740573
- OpenAlex
- W1913599140
- Cited by
- 167
- References
- 35
- Citations by year
- 2025: 3 · 2024: 6 · 2023: 2 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 1 · 2018: 1 · 2017: 4 · 2016: 4 · 2015: 5 · 2014: 8 · 2013: 9 · 2012: 8
- FWCI
- 6.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- NF-κB, Rel transcription factors, neuroprotection, neurodegeneration, forebrain neurons, transgenic mouse model, hippocampal slice cultures, neurodegenerative disease treatment
- MeSH terms
- NF-KappaB Inhibitor alpha, Animals, Enzyme Inhibitors, Gene Expression Regulation, Genes, Dominant, Hippocampus, Humans, Kainic Acid, Luminescent Proteins, Mice, Transgenic, Mutation, Neurons, Neurotoxins, Organ Specificity, Promoter Regions, Genetic, NF-kappa B, Prosencephalon, Cell Death, Calcium-Calmodulin-Dependent Protein Kinases, Transgenes, I-kappa B Proteins, Green Fluorescent Proteins, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2, In Vitro Techniques
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