ArticleProceedings of the National Academy of Sciences of the United States of America2012
Alternative pathway of cell death in Drosophila mediated by NF-κB transcription factor Relish.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Microbiome Integrity Protects Against Glial-Mediated Tau and Amyloid Pathology Through Circadian and Autophagy Homeostasis.bioRxiv : the preprint server for biology · 2026Article
- From retina to brain: retinal dysfunction and dopaminergic neurodegeneration inFrontiers in cell and developmental biology · 2026Article
- Pathogen-specific social immunity is associated with erosion of individual immune function in an ant.Nature communications · 2024Article
- The NF-κB Factor Relish maintains blood progenitor homeostasis in the developing Drosophila lymph gland.PLoS genetics · 2024Article
- Evaluation of Neuroinflammatory Contribution to Neurodegeneration in LRRK2Biomedicines · 2024Article
- Dysregulation of innate immune signaling in animal models of spinal muscular atrophy.BMC biology · 2024Article
- Dysregulation of innate immune signaling in animal models of Spinal Muscular Atrophy.bioRxiv : the preprint server for biology · 2023Article
- The circular RNA Edis regulates neurodevelopment and innate immunity.PLoS genetics · 2022Article
- Caspar, an adapter for VAPB and TER94, modulates the progression of ALS8 by regulating IMD/NFκB-mediated glial inflammation in a Drosophila model of human disease.Human molecular genetics · 2022Article
- Suppression of intestinal dysfunction in a Drosophila model of Parkinson's disease is neuroprotective.Nature aging · 2022Article
- Drosophila as a model to explore secondary injury cascades after traumatic brain injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Article
- NF-κB disinhibition contributes to dendrite defects in fly models of neurodegenerative diseases.The Journal of cell biology · 2020Article
- Survival Following Traumatic Brain Injury inGenetics · 2020Article
- Two Roles for theInsects · 2020Article
- Beyond Host Defense: Deregulation ofFrontiers in immunology · 2020Review
- Innate immune responses to paraquat exposure in a Drosophila model of Parkinson's disease.Scientific reports · 2019Article
- Review
- The NF-κB Factor Relish Regulates Atg1 Expression and Controls Autophagy.Cell reports · 2018Article
- Variation in Mitochondria-Derived Transcript Levels Associated With DDT Resistance in the 91-R Strain of Drosophila melanogaster (Diptera: Drosophilidae).Journal of insect science (Online) · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Photoreceptor cell death accompanying many retinal degenerative disorders results in irreversible loss of vision in humans. However, the precise molecular pathway that executes cell death is not known. Our results from a Drosophila model of retinal degeneration corroborate previously reported findings that the developmental apoptotic pathway is not involved in photoreceptor cell demise. By undertaking a candidate gene approach, we find that players involved in the immune response against gram-negative bacteria are involved in retinal degeneration. Here, we report that the NF-κB transcription factor Relish regulates neuronal cell death. Retinal degeneration is prevented in genetic backgrounds that block Relish activation. We also report that the N-terminal domain of Relish encodes unique toxic functions. These data uncover a unique molecular pathway of retinal degeneration in Drosophila and identify a previously unknown function of NF-κB signaling in cell death.
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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.