Component
Human high-affinity copper transporter CTR1 / SLC31A1
Human high-affinity copper transporter CTR1 / SLC31A1. Species, exposure and limitations are retained in each linked claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
CTR1-mediated radiocopper transport was energy independent and increased at acidic extracellular pH and high extracellular potassium in the assay.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/11734551.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c", "start_char": 0, "end_char": 1144, "text_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c"}
- experimental_model
- Human CTR1 expression and radiocopper transport assays
- exposure
- CTR1 expression; pH and potassium changes in culture
- limitations
- Transport kinetics in cells; elevated assay potassium is not evidence that potassium supplements improve human copper status.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human protein in human HEK293 cells
- plain_language
- The chemical surroundings changed transport speed; this is not a dietary potassium recommendation.
- primary_references
- [copper-p11734551] Biochemical characterization of the human copper transporter Ctr1. (2002). https://pubmed.ncbi.nlm.nih.gov/11734551/ DOI: 10.1074/jbc.m104728200
- tissue_or_cell_type
- Plasma membrane
- transport_effect
- raises The object already names cellular copper uptake.
- transport_pool
- the cytosol The object already names cellular copper uptake.
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 260–271
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CTR1 expression and radiocopper transport assays · source_derived_draft · unverified_draft
### copper-ctr1-energy-ph CTR1-mediated radiocopper transport was energy independent and increased at acidic extracellular pH and high extracellular potassium in the assay. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The chemical surroundings changed transport speed; this is not a dietary potassium recommendation. organism: Human protein in human HEK293 cells tissue_or_cell_type: Plasma membrane experimental_model: Human CTR1 expression and radiocopper transport assays limitations: Transport kinetics in cells; elevated assay potassium is not evidence that potassium supplements improve human copper status. exposure: CTR1 expression; pH and potassium changes in culture evidence_span: {"source_cache": "artifacts/copper-research/11734551.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c", "start_char": 0, "end_char": 1144, "text_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c"} [copper-p11734551] Biochemical characterization of the human copper transporter Ctr1. (2002). https://pubmed.ncbi.nlm.nih.gov/11734551/ DOI: 10.1074/jbc.m104728200
Complete structured claim and evidenceHuman CTR1 supported high-affinity, saturable, metal-selective copper uptake at the plasma membrane.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/11734551.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c", "start_char": 0, "end_char": 1144, "text_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c"}
- experimental_model
- Human CTR1 expression and radiocopper transport assays
- exposure
- CTR1 expression; pH and potassium changes in culture
- limitations
- Transport kinetics in cells; elevated assay potassium is not evidence that potassium supplements improve human copper status.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human protein in human HEK293 cells
- plain_language
- CTR1 is a controlled entry route for copper into cells.
- primary_references
- [copper-p11734551] Biochemical characterization of the human copper transporter Ctr1. (2002). https://pubmed.ncbi.nlm.nih.gov/11734551/ DOI: 10.1074/jbc.m104728200
- tissue_or_cell_type
- Plasma membrane
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 247–258
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CTR1 expression and radiocopper transport assays · source_derived_draft · unverified_draft
### copper-ctr1-uptake Human CTR1 supported high-affinity, saturable, metal-selective copper uptake at the plasma membrane. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: CTR1 is a controlled entry route for copper into cells. organism: Human protein in human HEK293 cells tissue_or_cell_type: Plasma membrane experimental_model: Human CTR1 expression and radiocopper transport assays limitations: Transport kinetics in cells; elevated assay potassium is not evidence that potassium supplements improve human copper status. exposure: CTR1 expression; pH and potassium changes in culture evidence_span: {"source_cache": "artifacts/copper-research/11734551.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c", "start_char": 0, "end_char": 1144, "text_sha256": "e7b07ef7169b07bef414cdfb8996cffda2636f9a1bcd93b556d22bdce980a03c"} [copper-p11734551] Biochemical characterization of the human copper transporter Ctr1. (2002). https://pubmed.ncbi.nlm.nih.gov/11734551/ DOI: 10.1074/jbc.m104728200
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.