ArticleCellular and molecular life sciences : CMLS2010
Optic atrophy 3 as a protein of the mitochondrial outer membrane induces mitochondrial fragmentation.
Article in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 64 citations in OpenAlex.
- Mitochondrial protein OPA3 sustains cardiac function by regulating calcium handling in male mice.Nature communications · 2026Article
- The role of hydrogen sulfide regulation of ferroptosis in different diseases.Apoptosis : an international journal on programmed cell death · 2024Review
- Mitochondria in Retinal Ganglion Cells: Unraveling the Metabolic Nexus and Oxidative Stress.International journal of molecular sciences · 2024Review
- Ethnicity-related differences in mitochondrial regulation by insulin stimulation in diabetes.Journal of cellular physiology · 2024Review
- Ovarian Cancer: A Landscape of Mitochondria with Emphasis on Mitochondrial Dynamics.International journal of molecular sciences · 2023Review
- Review
- Bi-allelic LETM1 variants perturb mitochondrial ion homeostasis leading to a clinical spectrum with predominant nervous system involvement.American journal of human genetics · 2022Article
- Expression status and prognostic significance of mitochondrial dynamics OPA3 in human ovarian cancer.Aging · 2022Article
- Sinonasal Inverted Papilloma and Squamous Cell Carcinoma: Contemporary Management and Patient Outcomes.Cancers · 2022Review
- MYB proto-oncogene like 2 promotes hepatocellular carcinoma growth and glycolysis via binding to theBioengineered · 2022Article
- Molecular Mechanisms behind Inherited Neurodegeneration of the Optic Nerve.Biomolecules · 2021Review
- The Role of Mitochondria in Optic Atrophy With Autosomal Inheritance.Frontiers in neuroscience · 2021Review
- Oncogenic K-ras Induces Mitochondrial OPA3 Expression to Promote Energy Metabolism in Pancreatic Cancer Cells.Cancers · 2019Article
- Mitochondrial Morphofunction in Mammalian Cells.Antioxidants & redox signaling · 2019Review
- Putative biomarkers of malignant transformation of sinonasal inverted papilloma into squamous cell carcinoma.The Journal of international medical research · 2019Article
- Autosomal dominant optic atrophy and cataract "plus" phenotype including axonal neuropathy.Neurology. Genetics · 2019Article
- Disorders of mitochondrial dynamics in peripheral neuropathy: Clues from hereditary neuropathy and diabetes.International review of neurobiology · 2019Review
- Intracellular vesicle trafficking plays an essential role in mitochondrial quality control.Molecular biology of the cell · 2018Article
- The Alterations in Mitochondrial DNA Copy Number and Nuclear-Encoded Mitochondrial Genes in Rat Brain Structures after Cocaine Self-Administration.Molecular neurobiology · 2017Article
- Optic atrophy, cataracts, lipodystrophy/lipoatrophy, and peripheral neuropathy caused by a de novoCold Spring Harbor molecular case studies · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The optic atrophy 3 (OPA3) gene, which has no known homolog or biological function, is mutated in patients with hereditary optic neuropathies. Here, we identified OPA3 as an integral protein of the mitochondrial outer membrane (MOM), with a C-terminus exposed to the cytosol and an N-terminal mitochondrial targeting domain. By quantitative analysis, we demonstrated that overexpression of OPA3 significantly induced mitochondrial fragmentation, whereas OPA3 knockdown resulted in highly elongated mitochondria. Cells with mitochondria fragmented by OPA3 did not undergo spontaneous apoptotic cell death, but were significantly sensitized to staurosporine- and TRAIL-induced apoptosis. In contrast, overexpression of a familial OPA3 mutant (G93S) induced mitochondrial fragmentation and spontaneous apoptosis, suggesting that OPA3 mutations may cause optic atrophy via a gain-of-function mechanism. Together, these results indicate that OPA3, as an integral MOM protein, has a crucial role in mitochondrial fission, and provides a direct link between mitochondrial morphology and optic atrophy.
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.