ArticleFrontiers in aging neuroscience2013
Role of the P-Type ATPases, ATP7A and ATP7B in brain copper homeostasis.
Article in Frontiers in aging neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 171 citations in OpenAlex.
- Effluxosomes and the evolution of metal resistance inInfection and immunity · 2026Review
- Zinc and Copper Metallic Instability: Investigating Altered Metal Functionality in both Human and Animal Studies.Biological trace element research · 2026Review
- Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases.MedComm · 2026Review
- 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
- Role of cuproptosis in digestive system tumors (Review).International journal of molecular medicine · 2026Review
- 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
- Agricultural Copper Pesticide Exposure and Metabolic Profiles among Parkinson's Disease Cases and Community Controls in California.Chemical research in toxicology · 2026Article
- Mechanisms and therapeutic strategies of copper homeostasis in the pathogenesis of sepsis-induced cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Generalized Dystonia in a Patient With Wilson Disease 5 Years After Liver Transplant: A Case Report.Tremor and other hyperkinetic movements (New York, N.Y.) · 2026Article
- Copper regulates the expression of immune genes in microglial cells in vitro.Immunobiology · 2025Article
- Copper homeostasis and cuproptosis in Alzheimer's disease (Review).International journal of molecular medicine · 2025Review
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- A primer on copper biology in the brain.Neurobiology of disease · 2025Review
- Caloric Restriction Mimetics as Priming Agents of Mesenchymal Stem Cells Secretome to Enhance Regenerative Responses to Parkinson's Disease.Molecules (Basel, Switzerland) · 2025Review
- Computational studies on the functional and structural impact of pathogenic mutations in enzymes.Protein science : a publication of the Protein Society · 2025Review
- Minimal Criteria to Screen for Wilson Disease: A Delphi Consensus in the United States.International journal of hepatology · 2025Article
- Unveiling the mechanistic nexus: how micronutrient enrichment shapes brain function, and cognitive health.Frontiers in molecular biosciences · 2025Review
- Alpha-synuclein null mutation exacerbates the phenotype of a model of Menkes disease in female mice.Frontiers in neuroscience · 2025Article
- Cuproptosis-related genes associated with mitochondrial dysfunction in Parkinson's disease.PloS one · 2025Article
- Cuproptosis Cell Death Molecular Events and Pathways to Liver Disease.Journal of inflammation research · 2025Review
21 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past two decades there have been significant advances in our understanding of copper homeostasis and the pathological consequences of copper dysregulation. Cumulative evidence is revealing a complex regulatory network of proteins and pathways that maintain copper homeostasis. The recognition of copper dysregulation as a key pathological feature in prominent neurodegenerative disorders such as Alzheimer's, Parkinson's, and prion diseases has led to increased research focus on the mechanisms controlling copper homeostasis in the brain. The copper-transporting P-type ATPases (copper-ATPases), ATP7A and ATP7B, are critical components of the copper regulatory network. Our understanding of the biochemistry and cell biology of these complex proteins has grown significantly since their discovery in 1993. They are large polytopic transmembrane proteins with six copper-binding motifs within the cytoplasmic N-terminal domain, eight transmembrane domains, and highly conserved catalytic domains. These proteins catalyze ATP-dependent copper transport across cell membranes for the metallation of many essential cuproenzymes, as well as for the removal of excess cellular copper to prevent copper toxicity. A key functional aspect of these copper transporters is their copper-responsive trafficking between the trans-Golgi network and the cell periphery. ATP7A- and ATP7B-deficiency, due to genetic mutation, underlie the inherited copper transport disorders, Menkes and Wilson diseases, respectively. Their importance in maintaining brain copper homeostasis is underscored by the severe neuropathological deficits in these disorders. Herein we will review and update our current knowledge of these copper transporters in the brain and the central nervous system, their distribution and regulation, their role in normal brain copper homeostasis, and how their absence or dysfunction contributes to disturbances in copper homeostasis and neurodegeneration.
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