ArticleThe Biochemical journal2002
Biochemical characterization and subcellular localization of human copper transporter 1 (hCTR1).
Article in The Biochemical journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 184 citations in OpenAlex.
- Balancing cellular copper levels via the post-translational regulation of copper transport.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Human CTR1 Through the Ages: Milestones and Emerging Roles in Disease and Therapy.Biomolecules · 2025Review
- Elevated intracellular copper induces CTR1 monomerization and prevents copper uptake.Nature communications · 2025Article
- Decreased Expression of theInternational journal of molecular sciences · 2022Article
- Copper deficiency affects the developmental competence of porcine oocytes maturedFrontiers in cell and developmental biology · 2022Article
- Crossroads between membrane trafficking machinery and copper homeostasis in the nerve system.Open biology · 2021Review
- Redox-Active Metal Ions and Amyloid-Degrading Enzymes in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Structural and Functional Diversity Among the Members of CTR, the Membrane Copper Transporter Family.The Journal of membrane biology · 2020Review
- Mammalian copper homeostasis requires retromer-dependent recycling of the high-affinity copper transporter 1.Journal of cell science · 2020Article
- Copper Sources for Sod1 Activation.Antioxidants (Basel, Switzerland) · 2020Review
- Promotion of cadmium uptake and cadmium-induced toxicity by the copper transporter CTR1 in HepG2 and ZFL cells.Toxicology reports · 2020Article
- Review
- X-ray structures of the high-affinity copper transporter Ctr1.Nature communications · 2019Article
- Article
- Reconstitution of a thermophilic CuThe Journal of biological chemistry · 2018Article
- The mitochondrial metallochaperone SCO1 maintains CTR1 at the plasma membrane to preserve copper homeostasis in the murine heart.Human molecular genetics · 2017Article
- Prognostic value of copper transporter 1 expression in patients with clear cell renal cell carcinoma.Oncology letters · 2017Article
- Gene duplication and neo-functionalization in the evolutionary and functional divergence of the metazoan copper transporters Ctr1 and Ctr2.The Journal of biological chemistry · 2017Article
- Accounting for Protein Subcellular Localization: A Compartmental Map of the Rat Liver Proteome.Molecular & cellular proteomics : MCP · 2017Article
- Copper transporters and chaperones: Their function on angiogenesis and cellular signalling.Journal of biosciences · 2016Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human copper transporter 1 gene (hCTR1) was previously identified by functional complementation in ctr1-deficient yeast. Overexpression of hCTR1 in wild-type yeast leads to increased sensitivity to copper toxicity, and mice with a homozygous disruption at the Ctr1 locus die early during embryogenesis. It is proposed that hCTR1 is responsible for high-affinity copper uptake into human cells, but the underlying molecular mechanisms are unknown. To begin to investigate the biochemical characteristics of hCTR1, a polyclonal antiserum was raised against recombinant hCTR1-fusion peptides. Biosynthetic studies using this antiserum revealed that hCTR1 was synthesized as a precursor protein of 28 kDa containing N-linked oligosaccharides, and is then converted to a mature protein of approx. 35 kDa, which is ubiquitously expressed. Immunofluorescence studies showed that subcellular hCTR1 localization differed markedly between cell types. In some cell lines, hCTR1 was located predominantly in an intracellular vesicular perinuclear compartment, and in others hCTR1 was located predominantly at the plasma membrane. In contrast with the copper export P-type ATPases mutated in Wilson disease and Menkes disease, the localization of hCTR1 was not influenced by copper concentrations. Inhibition of endocytosis by methyl-beta-cyclodextrin caused a partial redistribution of hCTR1 to the cell surface of HeLa cells. Taken together, the results in this study suggest a cell-specific control of copper uptake, which involves subcellular localization of the hCTR1 protein.
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