ArticleJournal of cell science2024
Regulation of the apico-basolateral trafficking polarity of the homologous copper-ATPases ATP7A and ATP7B.
Article in Journal of cell science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 21 citations in OpenAlex.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- AP-1B Controls Several Levels of Cell Proliferation and Differentiation in Mouse Enteroids.Biology of the cell · 2026Article
- Engineering cuproptosis with nanomedicine: Design, combination therapy, and translation in cancer.Materials today. Bio · 2026Review
- Copper in Human Health and Disease: Insights from Inherited Disorders.Physiology (Bethesda, Md.) · 2026Review
- Review
- Harnessing Cuproptosis resistance to advance cancer therapeutics.Apoptosis : an international journal on programmed cell death · 2026Review
- Cuproptosis in Sepsis: Cell Type-Specific Mechanisms and Clinical Prospects.Drug design, development and therapy · 2026Review
- Harnessing copper: Innovative approaches to combat neurodegenerative diseases and cancer (Review).International journal of molecular medicine · 2026Review
- The Copper Chaperone ATOX1 Exhibits Differential Protein-Protein Interactions and Contributes to Skeletal Myoblast Differentiation.Molecular and cellular biology · 2026Article
- Cuproptosis: a novel therapeutic mechanism in lung cancer.Cancer cell international · 2025Review
- Cuproptosis and cuproptosis-related cell death and genes: mechanistic links to spermatogenic cell death.Cell death discovery · 2025Review
- Mammalian copper homeostasis: physiological roles and molecular mechanisms.Physiological reviews · 2025Review
- Copper Metabolism-Related Genes as Biomarkers in Colon Adenoma and Cancer.International journal of general medicine · 2025Article
- Acute GARP depletion disrupts vesicle transport, leading to severe defects in sorting, secretion, and O-glycosylation.bioRxiv : the preprint server for biology · 2024Article
- Review
- The physiological and pathophysiological roles of copper in the nervous system.The European journal of neuroscience · 2024Review
- Copper Homeostasis in the Model OrganismCells · 2024Review
- Copper metabolism in osteoarthritis and its relation to oxidative stress and ferroptosis in chondrocytes.Frontiers in molecular biosciences · 2024Review
- Targeting cuproptosis with nano material: new way to enhancing the efficacy of immunotherapy in colorectal cancer.Frontiers in pharmacology · 2024Review
- Acute GARP Depletion Disrupts Vesicle Transport, Leading to Severe Defects in Sorting, Secretion and O-Glycosylation.Traffic (Copenhagen, Denmark)Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The homologous P-type copper-ATPases (Cu-ATPases) ATP7A and ATP7B are the key regulators of copper homeostasis in mammalian cells. In polarized epithelia, upon copper treatment, ATP7A and ATP7B traffic from the trans-Golgi network (TGN) to basolateral and apical membranes, respectively. We characterized the sorting pathways of Cu-ATPases between TGN and the plasma membrane and identified the machinery involved. ATP7A and ATP7B reside on distinct domains of TGN in limiting copper conditions, and in high copper, ATP7A traffics to basolateral membrane, whereas ATP7B traverses common recycling, apical sorting and apical recycling endosomes en route to apical membrane. Mass spectrometry identified regulatory partners of ATP7A and ATP7B that include the adaptor protein-1 complex. Upon knocking out pan-AP-1, sorting of both Cu-ATPases is disrupted. ATP7A loses its trafficking polarity and localizes on both apical and basolateral surfaces in high copper. By contrast, ATP7B loses TGN retention but retained its trafficking polarity to the apical domain, which became copper independent. Using isoform-specific knockouts, we found that the AP-1A complex provides directionality and TGN retention for both Cu-ATPases, whereas the AP-1B complex governs copper-independent trafficking of ATP7B solely. Trafficking phenotypes of Wilson disease-causing ATP7B mutants that disrupts putative ATP7B-AP1 interaction further substantiates the role of AP-1 in apical sorting of ATP7B.
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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.