Component

Human CUBN gene

Gene encoding cubilin; variants can impair endocytic vitamin-carrier retrieval.

1 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.

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. 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

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