ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
SLC30A10 is a cell surface-localized manganese efflux transporter, and parkinsonism-causing mutations block its intracellular trafficking and efflux activity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
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Who cites it
134 citing papers in PubMed, 205 citations in OpenAlex.
- Genome-wide association study of toxic metals and trace elements reveals novel associations.Human molecular genetics · 2015Trial
- Manganese availability determines insulin sensitivity by enhancing Akt activity.bioRxiv : the preprint server for biology · 2026Article
- Manganese: biology, physiology and role in disease.Cell discovery · 2026Review
- Overlaps in mammalian iron and manganese homeostasis: recent advances.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Evidence for a role of calcium and vitamin D in the regulation of manganese homeostasis and in the prevention or management of manganese-induced disease.American journal of physiology. Endocrinology and metabolism · 2026Article
- Neuron-specific modulation of SLC30A10 identifies dopaminergic and glutamatergic neurons as targets of manganese-induced motor disease.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Transcriptomics, identification, and testing of manganese metabolism-related genes in cervical squamous cell carcinoma.Frontiers in oncology · 2026Article
- Molecular mechanisms of SLC30A10-mediated manganese transport.Nature communications · 2025Article
- An iPSC-derived neuronal model reveals manganese's role in neuronal endocytosis, calcium flux and mitochondrial bioenergetics.iScience · 2025Article
- Systematic analysis of naturally occurring missense mutations in human manganese transporters: prediction and structural insights.bioRxiv : the preprint server for biology · 2025Article
- Manganese Neurotoxicity: A Comprehensive Review of Pathophysiology and Inherited and Acquired Disorders.Journal of xenobiotics · 2025Review
- Gut to brain: essential micronutrient and trace element manganese transport, function and toxicity.Frontiers in physiology · 2025Review
- Hypermagnesemia with Dystonia Type 2: Case Report of a New SLC30A10 Variant.Journal of pharmacy & bioallied sciences · 2024Article
- Forced Overexpression and Knockout Analysis of SLC30A and SLC39A Family Genes Suggests Their Involvement in Establishing Resistance to Cisplatin in Human Cancer Cells.International journal of molecular sciences · 2024Article
- ZIP8 Is Upregulated in the Testis ofNutrients · 2024Article
- Manganese: From Soil to Human Health-A Comprehensive Overview of Its Biological and Environmental Significance.Nutrients · 2024Review
- Exome Sequence Analysis to Characterize Undiagnosed Family Segregating Motor Impairment and Dystonia.Journal of clinical medicine · 2024Article
- A water-soluble, cell-permeable Mn(ii) sensor enables visualization of manganese dynamics in live mammalian cells.Chemical science · 2024Article
- Elevated thyroid manganese reduces thyroid iodine to induce hypothyroidism in mice, but not rats, lacking SLC30A10 transporter.Metallomics : integrated biometal science · 2024Article
- PHD2 enzyme is an intracellular manganese sensor that initiates the homeostatic response against elevated manganese.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
74 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Manganese (Mn) is an essential metal, but elevated cellular levels are toxic and may lead to the development of an irreversible parkinsonian-like syndrome that has no treatment. Mn-induced parkinsonism generally occurs as a result of exposure to elevated Mn levels in occupational or environmental settings. Additionally, patients with compromised liver function attributable to diseases, such as cirrhosis, fail to excrete Mn and may develop Mn-induced parkinsonism in the absence of exposure to elevated Mn. Recently, a new form of familial parkinsonism was reported to occur as a result of mutations in SLC30A10. The cellular function of SLC30A10 and the mechanisms by which mutations in this protein cause parkinsonism are unclear. Here, using a combination of mechanistic and functional studies in cell culture, Caenorhabditis elegans, and primary midbrain neurons, we show that SLC30A10 is a cell surface-localized Mn efflux transporter that reduces cellular Mn levels and protects against Mn-induced toxicity. Importantly, mutations in SLC30A10 that cause familial parkinsonism blocked the ability of the transporter to traffic to the cell surface and to mediate Mn efflux. Although expression of disease-causing SLC30A10 mutations were not deleterious by themselves, neurons and worms expressing these mutants exhibited enhanced sensitivity to Mn toxicity. Our results provide novel insights into the mechanisms involved in the onset of a familial form of parkinsonism and highlight the possibility of using enhanced Mn efflux as a therapeutic strategy for the potential management of Mn-induced parkinsonism, including that occurring as a result of mutations in SLC30A10.
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