ArticlePloS one2014
Loss of optineurin in vivo results in elevated cell death and alters axonal trafficking dynamics.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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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.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Axonopathy Underlying Amyotrophic Lateral Sclerosis: Unraveling Complex Pathways and Therapeutic Insights.Neuroscience bulletin · 2024Review
- Modelling amyotrophic lateral sclerosis in rodents.Nature reviews. Neuroscience · 2022Review
- Selective autophagy: the rise of the zebrafish model.Autophagy · 2021Review
- Autophagy in Drosophila and Zebrafish.Advances in experimental medicine and biology · 2021Article
- Review
- Review
- Dysfunction of Optineurin in Amyotrophic Lateral Sclerosis and Glaucoma.Frontiers in immunology · 2018Review
- Optineurin: A Coordinator of Membrane-Associated Cargo Trafficking and Autophagy.Frontiers in immunology · 2018Review
- Studying Autophagy in Zebrafish.Cells · 2017Review
- Mitophagy and Alzheimer's Disease: Cellular and Molecular Mechanisms.Trends in neurosciences · 2017Review
- From animal models to human disease: a genetic approach for personalized medicine in ALS.Acta neuropathologica communications · 2016Review
- Visual impairment in an optineurin mouse model of primary open-angle glaucoma.Neurobiology of aging · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in Optineurin have been associated with ALS, glaucoma, and Paget's disease of bone in humans, but little is known about how these mutations contribute to disease. Most of the cellular consequences of Optineurin loss have come from in vitro studies, and it remains unclear whether these same defects would be seen in vivo. To answer this question, we assessed the cellular consequences of Optineurin loss in zebrafish embryos to determine if they showed the same defects as have been described in the in vitro studies. We found that loss of Optineurin resulted in increased cell death, as well as subtle cell morphology, cell migration and vesicle trafficking defects. However, unlike experiments on cells in culture, we found no indication that the Golgi apparatus was disrupted or that NF-κB target genes were upregulated. Therefore, we conclude that in vivo loss of Optineurin shows some, but not all, of the defects seen in in vitro work.
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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.