ArticlePloS one2014
Impairment of Drosophila orthologs of the human orphan protein C19orf12 induces bang sensitivity and neurodegeneration.
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 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Therapeutic Advances in Major NBIA Disorders: Current Strategies and Translational Challenges.Neurology international · 2026Review
- Revealing the nervous system requirements of Alzheimer disease risk genes in Drosophila.American journal of human genetics · 2025Article
- Patient-Derived Neurons Exhibit α-Synuclein Pathology and Previously Unrecognized Major Histocompatibility Complex Class I Elevation in Mitochondrial Membrane Protein-Associated Neurodegeneration.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Iron Dysregulation in Neurodegeneration with Brain Iron Accumulation (NBIA): Links between Mutations Occurring in BPAN, PKAN, MPAN and PLAN Types and Iron Metabolism.Molecular neurobiology · 2025Review
- Loss of mouse C19orf12 homolog disturbs tubular ER homeostasis and leads to neuroaxonal dystrophy.Acta neuropathologica communications · 2025Article
- Revealing the nervous system requirements of Alzheimer's disease risk genes inbioRxiv : the preprint server for biology · 2025Article
- An Update and Perspectives on Mitochondrial Membrane Protein-Associated Neurodegeneration andBrain sciences · 2025Review
- Plastic Fly: WhatInternational journal of molecular sciences · 2024Article
- Nazo, the Drosophila homolog of the NBIA-mutated protein-c19orf12, is required for triglyceride homeostasis.PLoS genetics · 2024Article
- Identification of Autophagy as a Functional Target Suitable for the Pharmacological Treatment of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) In Vitro.Pharmaceutics · 2023Article
- C19orf12 ablation causes ferroptosis in mitochondrial membrane protein-associated with neurodegeneration.Free radical biology & medicine · 2022Article
- Emerging Disease-Modifying Therapies in Neurodegeneration With Brain Iron Accumulation (NBIA) Disorders.Frontiers in neurology · 2021Review
- Mitochondrial Dysfunction, Oxidative Stress and Neuroinflammation in Neurodegeneration with Brain Iron Accumulation (NBIA).Antioxidants (Basel, Switzerland) · 2020Review
- The Downregulation ofFrontiers in cell and developmental biology · 2020Article
- Parkinson's disease-associatedProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Neurodegeneration with Brain Iron Accumulation Disorders: Valuable Models Aimed at Understanding the Pathogenesis of Iron Deposition.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Review: Insights into molecular mechanisms of disease in neurodegeneration with brain iron accumulation: unifying theories.Neuropathology and applied neurobiology · 2016Review
- Mitochondrial dysfunction and defects in lipid homeostasis as therapeutic targets in neurodegeneration with brain iron accumulation.Rare diseases (Austin, Tex.) · 2016Article
- Defective lipid metabolism in neurodegeneration with brain iron accumulation (NBIA) syndromes: not only a matter of iron.Journal of inherited metabolic disease · 2015Review
- Mutations of C19orf12, coding for a transmembrane glycine zipper containing mitochondrial protein, cause mis-localization of the protein, inability to respond to oxidative stress and increased mitochondrial Ca²⁺.Frontiers in genetics · 2015Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the orphan gene C19orf12 were identified as a genetic cause in a subgroup of patients with NBIA, a neurodegenerative disorder characterized by deposits of iron in the basal ganglia. C19orf12 was shown to be localized in mitochondria, however, nothing is known about its activity and no functional link exists to the clinical phenotype of the patients. This situation led us to investigate the effects of C19orf12 down-regulation in the model organism Drosophila melanogaster. Two genes are present in D. melanogaster, which are orthologs of C19orf12, CG3740 and CG11671. Here we provide evidence that transgenic flies with impaired C19orf12 homologs reflect the neurodegenerative phenotype and represent a valid tool to further analyze the pathomechanism in C19orf12-associated NBIA.
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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.