ArticleMolecular biology reports2012
Overexpressed mutant optineurin(E50K) induces retinal ganglion cells apoptosis via the mitochondrial pathway.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Modeling human retinal ganglion cell axonal outgrowth, development, and pathology using pluripotent stem cell-based microfluidic platforms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Age-related effects of optineurin deficiency in the mouse eye.Vision research · 2024Article
- Retinal Ganglion Cells With a Glaucoma OPTN(E50K) Mutation Exhibit Neurodegenerative Phenotypes when Derived from Three-Dimensional Retinal Organoids.Stem cell reports · 2020Article
- The Protective Effect of Luteolin in Glucocorticoid-Induced Osteonecrosis of the Femoral Head.Frontiers in pharmacology · 2020Article
- Dysfunction of Optineurin in Amyotrophic Lateral Sclerosis and Glaucoma.Frontiers in immunology · 2018Review
- Chloride channel protein 2 prevents glutamate-induced apoptosis in retinal ganglion cells.Iranian journal of basic medical sciences · 2016Article
- Optineurin: The autophagy connection.Experimental eye research · 2016Review
- Induction of autophagy in rats upon overexpression of wild-type and mutant optineurin gene.BMC cell biology · 2015Article
- Optineurin regulates the interferon response in a cell cycle-dependent manner.PLoS pathogens · 2015Article
- Genetics of primary open angle glaucoma.Japanese journal of ophthalmology · 2014Review
- Article
- Brown fat determination and development from muscle precursor cells by novel action of bone morphogenetic protein 6.PloS one · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the coding region of the OPTN gene are associated with certain glaucomas. Although the function of the optineurin protein is yet to be elucidated, the most common mutation, E50K, is associated with a severe phenotype. Plasmids expressing wild-type Optineurin (WT) and mutant Optineurin(E50K) were transfected into RGC-5 and monitored by immunofluorescence staining and western blotting. The mutant Optineurin(E50K) induced the death of retinal ganglion cells by generation of reactive oxygen species accompanied disruption of mitochondrial transmembrane potential, down-regulation of bcl-2, and up-regulation of bax, which led to the release of cytochrome C from the mitochondria into the cytosol, which, in turn, resulted in the activation of caspase-9 and caspase-3, indicating that mutant Optineurin(E50K) acquired the ability to induce cell death through the mitochondrial caspase-dependent cell death pathway.
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