ArticleThe Journal of cell biology2020
NF-κB disinhibition contributes to dendrite defects in fly models of neurodegenerative diseases.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- From retina to brain: retinal dysfunction and dopaminergic neurodegeneration inFrontiers in cell and developmental biology · 2026Article
- Sortilin is associated with progranulin deficiency and autism-like behaviors in valproic acid-induced autism rats.CNS neuroscience & therapeutics · 2024Article
- Dysregulation of innate immune signaling in animal models of spinal muscular atrophy.BMC biology · 2024Article
- Regulated cell death and its role in Alzheimer's disease and amyotrophic lateral sclerosis.Acta neuropathologica · 2024Review
- Nuclear speckleopathies: developmental disorders caused by variants in genes encoding nuclear speckle proteins.Human genetics · 2024Review
- Dysregulation of innate immune signaling in animal models of Spinal Muscular Atrophy.bioRxiv : the preprint server for biology · 2023Article
- CBP-Mediated Acetylation of Importin α Mediates Calcium-Dependent Nucleocytoplasmic Transport of Selective Proteins inMolecules and cells · 2022Article
- A circular RNA Edis-Relish-castor axis regulates neuronal development in Drosophila.PLoS genetics · 2022Article
- C9orf72-associated arginine-rich dipeptide repeats induce RNA-dependent nuclear accumulation of Staufen in neurons.Human molecular genetics · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendrite pathology is frequently observed in various neurodegenerative diseases (NDs). Although previous studies identified several pathogenic mediators of dendrite defects that act through loss of function in NDs, the underlying pathogenic mechanisms remain largely unexplored. Here, our search for additional pathogenic contributors to dendrite defects in NDs identifies Relish/NF-κB as a novel gain-of-toxicity-based mediator of dendrite defects in animal models for polyglutamine (polyQ) diseases and amyotrophic lateral sclerosis (ALS). In a Drosophila model for polyQ diseases, polyQ-induced dendrite defects require Dredd/Caspase-8-mediated endoproteolytic cleavage of Relish to generate the N-terminal fragment, Rel68, and subsequent Charon-mediated nuclear localization of Rel68. Rel68 alone induced neuronal toxicity causing dendrite and behavioral defects, and we identify two novel transcriptional targets, Tup and Pros, that mediate Rel68-induced neuronal toxicity. Finally, we show that Rel68-induced toxicity also contributes to dendrite and behavioral defects in a Drosophila model for ALS. Collectively, our data propose disinhibition of latent toxicity of Relish/NF-κB as a novel pathogenic mechanism underlying dendrite pathology in NDs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.