Component

Mouse ceruloplasmin Cp

Mouse ceruloplasmin Cp. 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. Cp-null mice had impaired iron release from hepatocytes and reticuloendothelial cells, while measured iron absorption and plasma turnover were comparable to controls.

    Mouse ceruloplasmin Cp → Mouse release of stored iron from hepatocytes and reticuloendothelial cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/10485908.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067", "start_char": 0, "end_char": 1368, "text_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067"}
    experimental_model
    Ceruloplasmin gene disruption and ferrokinetics
    exposure
    Cp knockout followed through one year
    limitations
    Genetic ceruloplasmin absence differs from dietary copper shortage; normal intestinal absorption in this experiment does not imply all copper-deficient states absorb iron normally.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    The main defect was moving stored iron out of cells.
    primary_references
    [copper-p10485908] Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux. (1999). https://pubmed.ncbi.nlm.nih.gov/10485908/ DOI: 10.1073/pnas.96.19.10812
    tissue_or_cell_type
    Liver, spleen and reticuloendothelial cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 793–804

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ceruloplasmin gene disruption and ferrokinetics · source_derived_draft · unverified_draft

    ### copper-cp-iron-mobilization Cp-null mice had impaired iron release from hepatocytes and reticuloendothelial cells, while measured iron absorption and plasma turnover were comparable to controls. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The main defect was moving stored iron out of cells. organism: Mouse tissue_or_cell_type: Liver, spleen and reticuloendothelial cells experimental_model: Ceruloplasmin gene disruption and ferrokinetics limitations: Genetic ceruloplasmin absence differs from dietary copper shortage; normal intestinal absorption in this experiment does not imply all copper-deficient states absorb iron normally. exposure: Cp knockout followed through one year evidence_span: {"source_cache": "artifacts/copper-research/10485908.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067", "start_char": 0, "end_char": 1368, "text_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067"} [copper-p10485908] Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux. (1999). https://pubmed.ncbi.nlm.nih.gov/10485908/ DOI: 10.1073/pnas.96.19.10812
    Complete structured claim and evidence

  2. By one year, Cp-null mice had three- to sixfold higher liver and spleen iron with increased serum ferritin.

    Mouse ceruloplasmin Cp → 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/10485908.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067", "start_char": 0, "end_char": 1368, "text_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067"}
    experimental_model
    Ceruloplasmin gene disruption and ferrokinetics
    exposure
    Cp knockout followed through one year
    limitations
    Genetic ceruloplasmin absence differs from dietary copper shortage; normal intestinal absorption in this experiment does not imply all copper-deficient states absorb iron normally.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    High storage markers can coexist with an iron-distribution problem.
    primary_references
    [copper-p10485908] Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux. (1999). https://pubmed.ncbi.nlm.nih.gov/10485908/ DOI: 10.1073/pnas.96.19.10812
    tissue_or_cell_type
    Liver, spleen and reticuloendothelial cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 806–817

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ceruloplasmin gene disruption and ferrokinetics · source_derived_draft · unverified_draft

    ### copper-cp-liver-iron By one year, Cp-null mice had three- to sixfold higher liver and spleen iron with increased serum ferritin. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: High storage markers can coexist with an iron-distribution problem. organism: Mouse tissue_or_cell_type: Liver, spleen and reticuloendothelial cells experimental_model: Ceruloplasmin gene disruption and ferrokinetics limitations: Genetic ceruloplasmin absence differs from dietary copper shortage; normal intestinal absorption in this experiment does not imply all copper-deficient states absorb iron normally. exposure: Cp knockout followed through one year evidence_span: {"source_cache": "artifacts/copper-research/10485908.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067", "start_char": 0, "end_char": 1368, "text_sha256": "2feaccc19bf8f4480643a918de9300a6c224935b47c24e251d96050599e3b067"} [copper-p10485908] Targeted gene disruption reveals an essential role for ceruloplasmin in cellular iron efflux. (1999). https://pubmed.ncbi.nlm.nih.gov/10485908/ DOI: 10.1073/pnas.96.19.10812
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Whole-body Heph/Cp double-knockout mice developed severe anemia and low serum iron despite iron-loaded tissues.

    Mouse hephaestin Heph → Mouse circulating iron availability source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/30182051.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72", "start_char": 0, "end_char": 1882, "text_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72"}
    experimental_model
    Whole-body and intestine-specific Heph/Cp double-knockout mice
    exposure
    Combined or tissue-specific deletion; oral iron tracer
    limitations
    Double knockouts differ from low dietary copper. Detectable iron absorption remained, so these enzymes are not an absolute all-or-none gate for every absorption route.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    The body had iron, but much of it was in the wrong places.
    primary_references
    [copper-p30182051] Severe Iron Metabolism Defects in Mice With Double Knockout of the Multicopper Ferroxidases Hephaestin and Ceruloplasmin. (2018). https://pubmed.ncbi.nlm.nih.gov/30182051/ DOI: 10.1016/j.jcmgh.2018.06.006
    tissue_or_cell_type
    Intestine, liver, heart, pancreas and blood
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 819–830

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and intestine-specific Heph/Cp double-knockout mice · source_derived_draft · unverified_draft

    ### copper-heph-cp-low-blood-iron Whole-body Heph/Cp double-knockout mice developed severe anemia and low serum iron despite iron-loaded tissues. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The body had iron, but much of it was in the wrong places. organism: Mouse tissue_or_cell_type: Intestine, liver, heart, pancreas and blood experimental_model: Whole-body and intestine-specific Heph/Cp double-knockout mice limitations: Double knockouts differ from low dietary copper. Detectable iron absorption remained, so these enzymes are not an absolute all-or-none gate for every absorption route. exposure: Combined or tissue-specific deletion; oral iron tracer evidence_span: {"source_cache": "artifacts/copper-research/30182051.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72", "start_char": 0, "end_char": 1882, "text_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72"} [copper-p30182051] Severe Iron Metabolism Defects in Mice With Double Knockout of the Multicopper Ferroxidases Hephaestin and Ceruloplasmin. (2018). https://pubmed.ncbi.nlm.nih.gov/30182051/ DOI: 10.1016/j.jcmgh.2018.06.006
    Complete structured claim and evidence

  2. Whole-body double deletion loaded iron into duodenum, liver, heart and pancreas; intestine-specific Heph deletion with global Cp loss produced a more restricted distribution.

    Mouse hephaestin Heph → Mouse iron accumulation across multiple organs source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/30182051.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72", "start_char": 0, "end_char": 1882, "text_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72"}
    experimental_model
    Whole-body and intestine-specific Heph/Cp double-knockout mice
    exposure
    Combined or tissue-specific deletion; oral iron tracer
    limitations
    Double knockouts differ from low dietary copper. Detectable iron absorption remained, so these enzymes are not an absolute all-or-none gate for every absorption route.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Where the enzyme is missing changes where iron gets trapped.
    primary_references
    [copper-p30182051] Severe Iron Metabolism Defects in Mice With Double Knockout of the Multicopper Ferroxidases Hephaestin and Ceruloplasmin. (2018). https://pubmed.ncbi.nlm.nih.gov/30182051/ DOI: 10.1016/j.jcmgh.2018.06.006
    tissue_or_cell_type
    Intestine, liver, heart, pancreas and blood
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 832–843

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and intestine-specific Heph/Cp double-knockout mice · source_derived_draft · unverified_draft

    ### copper-heph-cp-organ-loading Whole-body double deletion loaded iron into duodenum, liver, heart and pancreas; intestine-specific Heph deletion with global Cp loss produced a more restricted distribution. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Where the enzyme is missing changes where iron gets trapped. organism: Mouse tissue_or_cell_type: Intestine, liver, heart, pancreas and blood experimental_model: Whole-body and intestine-specific Heph/Cp double-knockout mice limitations: Double knockouts differ from low dietary copper. Detectable iron absorption remained, so these enzymes are not an absolute all-or-none gate for every absorption route. exposure: Combined or tissue-specific deletion; oral iron tracer evidence_span: {"source_cache": "artifacts/copper-research/30182051.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72", "start_char": 0, "end_char": 1882, "text_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72"} [copper-p30182051] Severe Iron Metabolism Defects in Mice With Double Knockout of the Multicopper Ferroxidases Hephaestin and Ceruloplasmin. (2018). https://pubmed.ncbi.nlm.nih.gov/30182051/ DOI: 10.1016/j.jcmgh.2018.06.006
    Complete structured claim and evidence

  3. Both Heph/Cp double-knockout models still absorbed oral iron tracer, but retained an abnormally high fraction in the liver.

    Mouse hephaestin Heph → Mouse intestinal iron absorption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/copper-research/30182051.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72", "start_char": 0, "end_char": 1882, "text_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72"}
    experimental_model
    Whole-body and intestine-specific Heph/Cp double-knockout mice
    exposure
    Combined or tissue-specific deletion; oral iron tracer
    limitations
    Double knockouts differ from low dietary copper. Detectable iron absorption remained, so these enzymes are not an absolute all-or-none gate for every absorption route.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse
    plain_language
    Absorption and useful distribution are different steps.
    primary_references
    [copper-p30182051] Severe Iron Metabolism Defects in Mice With Double Knockout of the Multicopper Ferroxidases Hephaestin and Ceruloplasmin. (2018). https://pubmed.ncbi.nlm.nih.gov/30182051/ DOI: 10.1016/j.jcmgh.2018.06.006
    tissue_or_cell_type
    Intestine, liver, heart, pancreas and blood
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 845–856

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Whole-body and intestine-specific Heph/Cp double-knockout mice · source_derived_draft · unverified_draft

    ### copper-heph-cp-residual-absorption Both Heph/Cp double-knockout models still absorbed oral iron tracer, but retained an abnormally high fraction in the liver. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: Absorption and useful distribution are different steps. organism: Mouse tissue_or_cell_type: Intestine, liver, heart, pancreas and blood experimental_model: Whole-body and intestine-specific Heph/Cp double-knockout mice limitations: Double knockouts differ from low dietary copper. Detectable iron absorption remained, so these enzymes are not an absolute all-or-none gate for every absorption route. exposure: Combined or tissue-specific deletion; oral iron tracer evidence_span: {"source_cache": "artifacts/copper-research/30182051.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72", "start_char": 0, "end_char": 1882, "text_sha256": "57ed2ee0540cc9ec88748eaa23af1a38d307271d9e7ea6367a24d412622a4b72"} [copper-p30182051] Severe Iron Metabolism Defects in Mice With Double Knockout of the Multicopper Ferroxidases Hephaestin and Ceruloplasmin. (2018). https://pubmed.ncbi.nlm.nih.gov/30182051/ DOI: 10.1016/j.jcmgh.2018.06.006
    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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