ArticleThe Journal of biological chemistry2018
ATP7A and ATP7B copper transporters have distinct functions in the regulation of neuronal dopamine-β-hydroxylase.
Article in The Journal of biological chemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- Copper Dysregulation in Major Depression: A Systematic Review and Meta-Analytic Evidence for a Putative Trait Marker.International journal of molecular sciences · 2025Pooled it
- A reproducible and physiologically relevant human iPSC-derived platform for in vitro modeling of the neurocardiac junction.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Copper import via CTR1 supports the β3-Adrenergic thermogenic program.Molecular metabolism · 2026Article
- Review
- Emerging role of copper in the pathophysiology of spinal cord injury.Neural regeneration research · 2026Article
- Allelic variation in the ATP7B gene promoter. Implications for phenotype variability, neurodegeneration and Pt resistance in tumor diseases.Journal of human genetics · 2026Article
- ATP7A-fibulin-4 complex delivers copper in the Golgi to activate LOX in renal fibrosis.JCI insight · 2026Article
- The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Copper Import via CTR1 Supports the β3-Adrenergic Thermogenic Program.bioRxiv : the preprint server for biology · 2026Article
- Distinct signaling mechanisms and proteome phenotypes are elicited by compartment-specific genetic defects of copper homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Metal Ions Within the Neuro-Immune-Tumor Axis.Journal of immunology research · 2026Review
- Nutrients and bioactive compounds as modifiers of neurodegenerative trajectories: molecular mechanisms, translational barriers, and precision nutrition.Frontiers in nutrition · 2026Review
- Copper regulates the expression of immune genes in microglial cells in vitro.Immunobiology · 2025Article
- Advances in Mammalian Metallomics: New Insights into Metal Dynamics and Biological Significance.International journal of molecular sciences · 2025Review
- RAD23B acquires a copper metalloadaptor function in amphibian-to-reptile evolution to increase metabolism and regulate genomic integrity.Molecular cell · 2025Article
- Copper and hepatic lipid dysregulation: Mechanisms and implications.World journal of hepatology · 2025Review
- Deep learning to assess erythritol in zebrafish development, circadian rhythm, and cardiovascular disease risk.NPJ science of food · 2025Article
- Bioactive polydopamine nanomedicines-assisted cancer immunotherapy.Materials today. Bio · 2025Review
- Computational studies on the functional and structural impact of pathogenic mutations in enzymes.Protein science : a publication of the Protein Society · 2025Review
- Copper homeostasis and pregnancy complications: a comprehensive review.Journal of assisted reproduction and genetics · 2025Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The copper (Cu) transporters ATPase copper-transporting alpha (ATP7A) and ATPase copper-transporting beta (ATP7B) are essential for the normal function of the mammalian central nervous system. Inactivation of ATP7A or ATP7B causes the severe neurological disorders, Menkes disease and Wilson disease, respectively. In both diseases, Cu imbalance is associated with abnormal levels of the catecholamine-type neurotransmitters dopamine and norepinephrine. Dopamine is converted to norepinephrine by dopamine-β-hydroxylase (DBH), which acquires its essential Cu cofactor from ATP7A. However, the role of ATP7B in catecholamine homeostasis is unclear. Here, using immunostaining of mouse brain sections and cultured cells, we show that DBH-containing neurons express both ATP7A and ATP7B. The two transporters are located in distinct cellular compartments and oppositely regulate the export of soluble DBH from cultured neuronal cells under resting conditions. Down-regulation of ATP7A, overexpression of ATP7B, and pharmacological Cu depletion increased DBH retention in cells. In contrast, ATP7B inactivation elevated extracellular DBH. Proteolytic processing and the specific activity of exported DBH were not affected by changes in ATP7B levels. These results establish distinct regulatory roles for ATP7A and ATP7B in neuronal cells and explain, in part, the lack of functional compensation between these two transporters in human disorders of Cu imbalance.
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Registered trials
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