Component

Mouse copper transporter Ctr1 / Slc31a1

Mouse copper transporter Ctr1 / Slc31a1. Species, exposure and limitations are retained in each linked claim.

5 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Mice lacking intestinal Ctr1 developed hepatic iron overload alongside systemic copper deficiency.

    Mouse copper transporter Ctr1 / Slc31a1 → Mouse hepatic iron accumulation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"}
    experimental_model
    Intestinal epithelial Ctr1 knockout mice
    exposure
    Intestinal Ctr1 deletion; postnatal copper rescue
    limitations
    Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    A copper transport defect also disrupted where iron accumulated.
    primary_references
    [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    tissue_or_cell_type
    Intestine and peripheral organs
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 325–336

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal epithelial Ctr1 knockout mice · source_derived_draft · unverified_draft

    ### copper-intestinal-ctr1-iron Mice lacking intestinal Ctr1 developed hepatic iron overload alongside systemic copper deficiency. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A copper transport defect also disrupted where iron accumulated. organism: Mouse tissue_or_cell_type: Intestine and peripheral organs experimental_model: Intestinal epithelial Ctr1 knockout mice limitations: Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose. exposure: Intestinal Ctr1 deletion; postnatal copper rescue evidence_span: {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"} [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    Complete structured claim and evidence

  2. Intestinal Ctr1 deletion reduced peripheral copper availability and caused neonatal growth failure and cardiac hypertrophy in mice.

    Mouse copper transporter Ctr1 / Slc31a1 → Delivery of intestinal copper to peripheral tissues source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"}
    experimental_model
    Intestinal epithelial Ctr1 knockout mice
    exposure
    Intestinal Ctr1 deletion; postnatal copper rescue
    limitations
    Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Copper in food is not enough if the intestine cannot deliver it to the body.
    primary_references
    [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    tissue_or_cell_type
    Intestine and peripheral organs
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 312–323

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal epithelial Ctr1 knockout mice · source_derived_draft · unverified_draft

    ### copper-intestinal-ctr1-systemic Intestinal Ctr1 deletion reduced peripheral copper availability and caused neonatal growth failure and cardiac hypertrophy in mice. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper in food is not enough if the intestine cannot deliver it to the body. organism: Mouse tissue_or_cell_type: Intestine and peripheral organs experimental_model: Intestinal epithelial Ctr1 knockout mice limitations: Genetic intestinal transport failure differs from low dietary intake. The indexed abstract does not establish the administration route of the rescue dose. exposure: Intestinal Ctr1 deletion; postnatal copper rescue evidence_span: {"source_cache": "artifacts/copper-research/16950140.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98", "start_char": 0, "end_char": 1026, "text_sha256": "08532f69fd9530033f8d9afcece9249fc50dd425f57313e120f55ea81cee8f98"} [copper-p16950140] Ctr1 drives intestinal copper absorption and is essential for growth, iron metabolism, and neonatal cardiac function. (2006). https://pubmed.ncbi.nlm.nih.gov/16950140/ DOI: 10.1016/j.cmet.2006.08.009
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Dietary copper limitation increased total and apically localized Ctr1 protein in mouse intestine.

    Copper → Mouse intestinal apical Ctr1 protein abundance source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/20699218.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012", "start_char": 0, "end_char": 1749, "text_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012"}
    experimental_model
    Intestinal immunolocalization and dietary copper limitation
    exposure
    Copper limitation in mice
    limitations
    Apical Ctr1 was observed in the examined mammalian preparations; membrane localization is model dependent and cannot be assigned universally to every human intestinal condition.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse, rat and pig; human HEK293T cells for separate processing experiments
    plain_language
    The intestine increased an entry route when copper supply fell.
    primary_references
    [copper-p20699218] Ctr1 is an apical copper transporter in mammalian intestinal epithelial cells in vivo that is controlled at the level of protein stability. (2010). https://pubmed.ncbi.nlm.nih.gov/20699218/ DOI: 10.1074/jbc.m110.143826
    tissue_or_cell_type
    Intestinal epithelium

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 351–362

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal immunolocalization and dietary copper limitation · source_derived_draft · unverified_draft

    ### copper-ctr1-intestinal-adaptation Dietary copper limitation increased total and apically localized Ctr1 protein in mouse intestine. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intestine increased an entry route when copper supply fell. organism: Mouse, rat and pig; human HEK293T cells for separate processing experiments tissue_or_cell_type: Intestinal epithelium experimental_model: Intestinal immunolocalization and dietary copper limitation limitations: Apical Ctr1 was observed in the examined mammalian preparations; membrane localization is model dependent and cannot be assigned universally to every human intestinal condition. exposure: Copper limitation in mice evidence_span: {"source_cache": "artifacts/copper-research/20699218.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012", "start_char": 0, "end_char": 1749, "text_sha256": "c638594d4e707bb39a8f2e8c1fed15a42982e1dc4d525fda112d28281a853012"} [copper-p20699218] Ctr1 is an apical copper transporter in mammalian intestinal epithelial cells in vivo that is controlled at the level of protein stability. (2010). https://pubmed.ncbi.nlm.nih.gov/20699218/ DOI: 10.1074/jbc.m110.143826
    Complete structured claim and evidence

  2. Oral elesclomol without extra copper supplementation rescued neonatal mortality in intestine-specific Ctr1 knockout mice.

    Elesclomol → Delivery of intestinal copper to peripheral tissues source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/35433682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617", "start_char": 0, "end_char": 1449, "text_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617"}
    experimental_model
    Oral elesclomol in genetically copper-transport-defective animals
    exposure
    Oral drug exposure without additional copper supplementation
    limitations
    Animal rescue does not establish safety or efficacy in people. Intestinal CTR1 loss is a different block from mitochondrial SLC25A3 loss.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse; separate Caenorhabditis elegans experiments
    plain_language
    The drug helped use existing dietary copper despite a missing intestinal entry route.
    primary_references
    [copper-p35433682] Oral Elesclomol Treatment Alleviates Copper Deficiency in Animal Models. (2022). https://pubmed.ncbi.nlm.nih.gov/35433682/ DOI: 10.3389/fcell.2022.856300
    tissue_or_cell_type
    Intestine and whole-animal development
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 598–609

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral elesclomol in genetically copper-transport-defective animals · source_derived_draft · unverified_draft

    ### copper-elesclomol-intestinal-bypass Oral elesclomol without extra copper supplementation rescued neonatal mortality in intestine-specific Ctr1 knockout mice. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug helped use existing dietary copper despite a missing intestinal entry route. organism: Mouse; separate Caenorhabditis elegans experiments tissue_or_cell_type: Intestine and whole-animal development experimental_model: Oral elesclomol in genetically copper-transport-defective animals limitations: Animal rescue does not establish safety or efficacy in people. Intestinal CTR1 loss is a different block from mitochondrial SLC25A3 loss. exposure: Oral drug exposure without additional copper supplementation evidence_span: {"source_cache": "artifacts/copper-research/35433682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617", "start_char": 0, "end_char": 1449, "text_sha256": "6ebf1fdc967be53f455383e4edc79468266a5685db3867ca04ce2e2ccc4f2617"} [copper-p35433682] Oral Elesclomol Treatment Alleviates Copper Deficiency in Animal Models. (2022). https://pubmed.ncbi.nlm.nih.gov/35433682/ DOI: 10.3389/fcell.2022.856300
    Complete structured claim and evidence

  3. The truncated Ctr1 form mobilized endosomal copper stores, whereas full-length Ctr1 efficiently supported plasma-membrane uptake.

    Mouse Ctr1 with cleaved extracellular N-terminal domain → Mobilization of copper from endosomal stores source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/24167251.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7315e9041dddd5510d6efd970560c80316d38120ba1d8eefca10952be8ea0968", "start_char": 0, "end_char": 1212, "text_sha256": "7315e9041dddd5510d6efd970560c80316d38120ba1d8eefca10952be8ea0968"}
    experimental_model
    Ctr2 knockout and Ctr1 processing experiments
    exposure
    Ctr2 deletion
    limitations
    CTR2 regulates truncated CTR1 and intracellular mobilization; it should not simply be treated as a duplicate plasma-membrane CTR1 importer.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Copper trapped inside a compartment needs a different access step.
    primary_references
    [copper-p24167251] Ctr2 regulates biogenesis of a cleaved form of mammalian Ctr1 metal transporter lacking the copper- and cisplatin-binding ecto-domain. (2013). https://pubmed.ncbi.nlm.nih.gov/24167251/ DOI: 10.1073/pnas.1311749110
    tissue_or_cell_type
    Endosomal stores versus plasma-membrane uptake

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 481–492

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ctr2 knockout and Ctr1 processing experiments · source_derived_draft · unverified_draft

    ### copper-truncated-ctr1-endosome The truncated Ctr1 form mobilized endosomal copper stores, whereas full-length Ctr1 efficiently supported plasma-membrane uptake. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Copper trapped inside a compartment needs a different access step. organism: Mouse tissue_or_cell_type: Endosomal stores versus plasma-membrane uptake experimental_model: Ctr2 knockout and Ctr1 processing experiments limitations: CTR2 regulates truncated CTR1 and intracellular mobilization; it should not simply be treated as a duplicate plasma-membrane CTR1 importer. exposure: Ctr2 deletion evidence_span: {"source_cache": "artifacts/copper-research/24167251.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7315e9041dddd5510d6efd970560c80316d38120ba1d8eefca10952be8ea0968", "start_char": 0, "end_char": 1212, "text_sha256": "7315e9041dddd5510d6efd970560c80316d38120ba1d8eefca10952be8ea0968"} [copper-p24167251] Ctr2 regulates biogenesis of a cleaved form of mammalian Ctr1 metal transporter lacking the copper- and cisplatin-binding ecto-domain. (2013). https://pubmed.ncbi.nlm.nih.gov/24167251/ DOI: 10.1073/pnas.1311749110
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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