Component

Human vitamin D-binding protein / GC

Human circulating carrier for vitamin D sterols, including D3 and calcifediol. Study-defined Human vitamin D-binding protein / GC. Read each linked record for species, exposure and endpoint.

3 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. Vitamin D-binding protein preferentially translocated thermally formed cholecalciferol from the skin into circulation in the reported photochemistry experiments.

    Human vitamin D-binding protein / GC → Entry of skin-generated cholecalciferol into circulation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary abstract; skin photochemistry and transport experiments.
    experimental_model
    Human skin-to-circulation vitamin transport
    exposure
    After UV generation and thermal conversion; quantitative carrier concentrations unavailable in abstract.
    limitations
    Preferential transport is not proof that every route of D3 entry requires DBP.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    A carrier helps newly made D3 enter the blood.
    primary_references
    [holick1980] Photosynthesis of previtamin D3 in human skin and the physiologic consequences. (1980). https://pubmed.ncbi.nlm.nih.gov/6251551/ DOI: 10.1126/science.6251551
    tissue_or_cell_type
    skin and circulation

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 121–134

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human skin-to-circulation vitamin transport · source_derived_draft · unverified_draft

    ### vd-act-dbp-skin-export Vitamin D-binding protein preferentially translocated thermally formed cholecalciferol from the skin into circulation in the reported photochemistry experiments. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A carrier helps newly made D3 enter the blood. organism: Homo sapiens tissue_or_cell_type: skin and circulation experimental_model: Human skin-to-circulation vitamin transport limitations: Preferential transport is not proof that every route of D3 entry requires DBP. exposure: After UV generation and thermal conversion; quantitative carrier concentrations unavailable in abstract. cross_nutrient: false evidence_location: Primary abstract; skin photochemistry and transport experiments. nutrient: Vitamin D2 and D3 [holick1980] Photosynthesis of previtamin D3 in human skin and the physiologic consequences. (1980). https://pubmed.ncbi.nlm.nih.gov/6251551/ DOI: 10.1126/science.6251551
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Human patients with mutations causing cubilin dysfunction excreted calcifediol in urine, supporting the cubilin-dependent renal carrier-retrieval pathway.

    Human CUBN gene → Urinary loss of calcifediol source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Primary abstract, cubilin sequestration and human urinary loss.
    experimental_model
    Human inherited cubilin dysfunction; supporting receptor experiments
    exposure
    Inherited CUBN dysfunction; patient details/doses not specified in retrieved abstract.
    limitations
    This shared B12/D transport machinery does not mean dietary B12 deficiency causes urinary D loss. Genotype-phenotype evidence is observational.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    Cubilin defects can cause loss of vitamin D precursor through urine.
    primary_references
    [nykjaer2001] Cubilin dysfunction causes abnormal metabolism of the steroid hormone 25(OH) vitamin D(3). (2001). https://pubmed.ncbi.nlm.nih.gov/11717447/ DOI: 10.1073/pnas.241516998
    tissue_or_cell_type
    kidney proximal tubule and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 257–270

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human inherited cubilin dysfunction; supporting receptor experiments · source_derived_draft · unverified_draft

    ### vd-act-cubilin-human-loss Human patients with mutations causing cubilin dysfunction excreted calcifediol in urine, supporting the cubilin-dependent renal carrier-retrieval pathway. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cubilin defects can cause loss of vitamin D precursor through urine. organism: Homo sapiens tissue_or_cell_type: kidney proximal tubule and urine experimental_model: Human inherited cubilin dysfunction; supporting receptor experiments limitations: This shared B12/D transport machinery does not mean dietary B12 deficiency causes urinary D loss. Genotype-phenotype evidence is observational. exposure: Inherited CUBN dysfunction; patient details/doses not specified in retrieved abstract. cross_nutrient: true evidence_location: Primary abstract, cubilin sequestration and human urinary loss. nutrient: Vitamin D2 and D3 [nykjaer2001] Cubilin dysfunction causes abnormal metabolism of the steroid hormone 25(OH) vitamin D(3). (2001). https://pubmed.ncbi.nlm.nih.gov/11717447/ DOI: 10.1073/pnas.241516998
    Complete structured claim and evidence

  2. Higher plasma DBP concentration was associated with longer 25(OH)D3 half-life in the combined model (0.04 days per 1 mg/L DBP; P=0.02); the corresponding 25(OH)D2 association was 0.03 days (P=0.03).

    Plasma vitamin D binding protein concentration → Plasma 25-hydroxyvitamin D3 tracer half-life source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Oral deuterated 25(OH)D2 and 25(OH)D3 tracer study; 18 Gambian and 18 UK healthy men
    exposure
    Oral deuterated 25(OH)D2 and 25(OH)D3, 40 nmol each; sampling 33 days.
    limitations
    Measured metabolites rather than parent supplements; country subgroup and DBP associations do not provide a universal whole-body storage half-life.
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    Carrier abundance was associated with metabolite persistence; it was not experimentally assigned.
    primary_references
    [jones2014] 25(OH)D2 half-life is shorter than 25(OH)D3 half-life and is influenced by DBP concentration and genotype. (2014). https://pubmed.ncbi.nlm.nih.gov/24885631/ DOI: 10.1210/jc.2014-1714
    tissue_or_cell_type
    Human circulating measurements
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1392–1403

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral deuterated 25(OH)D2 and 25(OH)D3 tracer study; 18 Gambian and 18 UK healthy men · source_derived_draft · unverified_draft

    ### vd-jones-dbp-half-life Higher plasma DBP concentration was associated with longer 25(OH)D3 half-life in the combined model (0.04 days per 1 mg/L DBP; P=0.02); the corresponding 25(OH)D2 association was 0.03 days (P=0.03). Condition category: biomarker_context nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Carrier abundance was associated with metabolite persistence; it was not experimentally assigned. organism: Homo sapiens tissue_or_cell_type: Human circulating measurements experimental_model: Oral deuterated 25(OH)D2 and 25(OH)D3 tracer study; 18 Gambian and 18 UK healthy men limitations: Measured metabolites rather than parent supplements; country subgroup and DBP associations do not provide a universal whole-body storage half-life. exposure: Oral deuterated 25(OH)D2 and 25(OH)D3, 40 nmol each; sampling 33 days. cross_nutrient: false [jones2014] 25(OH)D2 half-life is shorter than 25(OH)D3 half-life and is influenced by DBP concentration and genotype. (2014). https://pubmed.ncbi.nlm.nih.gov/24885631/ DOI: 10.1210/jc.2014-1714
    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.

    Evidence, AI assistance and curation standards