ArticleScientific reports2017
NF-κB regulates neuronal ankyrin-G via a negative feedback loop.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Tsc1 deletion in Purkinje neurons disrupts the axon initial segment, impairing excitability and cerebellar function.Neurobiology of disease · 2025Article
- Article
- Therapeutic strategies to recover ependymal barrier after inflammatory damage: relevance for recovering neurogenesis during development.Frontiers in neuroscience · 2023Review
- Risk of migraine contributed by genetic polymorphisms of ANKDD1B gene: a case-control study based on Chinese Han population.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- Cellular Specificity of NF-κB Function in the Nervous System.Frontiers in immunology · 2019Review
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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
The axon initial segment (AIS) is a neuronal compartment defined by ankyrin-G expression. We here demonstrate that the IKK-complex co-localizes and interacts with the cytoskeletal anchor protein ankyrin-G in immunoprecipitation and proximity-ligation experiments in cortical neurons. Overexpression of the 270 kDa variant of ankyrin-G suppressed, while gene-silencing of ankyrin-G expression increased nuclear factor-κB (NF-κB) activity in primary neurons, suggesting that ankyrin-G sequesters the transcription factor in the AIS. We also found that p65 bound to the ank3 (ankyrin-G) promoter sequence in chromatin immunoprecipitation analyses thereby increasing ank3 expression and ankyrin-G levels at the AIS. Gene-silencing of p65 or ankyrin-G overexpression suppressed ank3 reporter activity. Collectively these data demonstrate that p65/NF-κB controls ankyrin-G levels via a negative feedback loop, thereby linking NF-κB signaling with neuronal polarity and axonal plasticity.
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Registered trials
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