ArticleGenetics2015
A neuroprotective function of NSF1 sustains autophagy and lysosomal trafficking in Drosophila.
Article in Genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 18 citations in OpenAlex.
- The role of synaptic protein NSF in the development and progression of neurological diseases.Frontiers in neuroscience · 2024Review
- MitoSNARE Assembly and Disassembly Factors Regulate Basal Autophagy and Aging inInternational journal of molecular sciences · 2023Article
- Genetic modifiers of synucleinopathies-lessons from experimental models.Oxford open neuroscience · 2023Review
- Analysis ofBioMed research international · 2023Article
- DnaJC7 in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2022Review
- Functional Screening of Parkinson's Disease Susceptibility Genes to Identify Novel Modulators of α-Synuclein Neurotoxicity inFrontiers in aging neuroscience · 2022Article
- Modeling Neurodegenerative Disorders inInternational journal of molecular sciences · 2020Review
- De novo NSF mutations cause early infantile epileptic encephalopathy.Annals of clinical and translational neurology · 2019Article
- Neurodegeneration and locomotor dysfunction inJournal of cell science · 2018Article
- Article
- The crucial impact of lysosomes in aging and longevity.Ageing research reviews · 2016Review
- β-Guanidinopropionic acid extends the lifespan of Drosophila melanogaster via an AMP-activated protein kinase-dependent increase in autophagy.Aging cell · 2015Article
- Transcellular spreading of huntingtin aggregates in the Drosophila brain.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Death following traumatic brain injury in Drosophila is associated with intestinal barrier dysfunction.eLife · 2015Article
- The ubiquitin ligase Ariadne-1 regulates neurotransmitter release via ubiquitination of NSF.The Journal of biological chemistryArticle
- The effects of hyperbaric oxygen therapy on neuropathic pain via mitophagy in microglia.Molecular painArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A common feature of many neurodegenerative diseases is the accumulation of toxic proteins that disrupt vital cellular functions. Degradative pathways such as autophagy play an important protective role in breaking down misfolded and long-lived proteins. Neurons are particularly vulnerable to defects in these pathways, but many of the details regarding the link between autophagy and neurodegeneration remain unclear. We previously found that temperature-sensitive paralytic mutants in Drosophila are enriched for those exhibiting age-dependent neurodegeneration. Here we show that one of these mutants, comatose (comt), in addition to locomotor defects, displays shortened lifespan and progressive neurodegeneration, including loss of dopaminerigic (DA) neurons. comt encodes N-ethyl-maleimide sensitive fusion protein (NSF1), which has a well-documented role in synaptic transmission. However, the neurodegenerative phenotypes we observe in comt mutants do not appear to depend on defects in synaptic transmission, but rather from their inability to sustain autophagy under stress, due at least in part to a defect in trafficking of lysosomal proteases such as cathepsin-L. Conversely, overexpression of NSF1 rescues α-synuclein-induced toxicity of DA neurons in a model of Parkinson's disease. Our results demonstrate a neuroprotective role for NSF1 that involves mediation of fusion events crucial for degradative pathways such as autophagy, providing greater understanding of cellular dysfunctions common to several neurodegenerative diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.