Component

Mouse megalin / Lrp2

Mouse megalin / Lrp2

4 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. Megalin-mediated endocytosis retrieved filtered vitamin D-binding-protein/calcifediol complexes in proximal tubules.

    Mouse megalin / Lrp2 → Renal reclamation of filtered calcifediol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary abstract, receptor-mediated uptake and knockout phenotype.
    experimental_model
    Mouse renal endocytosis experiments
    exposure
    Endogenous carrier complexes and uptake assays; timing not specified in abstract.
    limitations
    Renal endocytosis finding does not exclude free-hormone uptake elsewhere.
    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
    Mus musculus
    plain_language
    Kidney cells reclaim carrier-bound D3 precursor from the filtrate.
    primary_references
    [nykjaer1999] An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3. (1999). https://pubmed.ncbi.nlm.nih.gov/10052453/ DOI: 10.1016/s0092-8674(00)80655-8
    tissue_or_cell_type
    kidney proximal tubule

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 227–240

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse renal endocytosis experiments · source_derived_draft · unverified_draft

    ### vd-act-megalin-retrieval Megalin-mediated endocytosis retrieved filtered vitamin D-binding-protein/calcifediol complexes in proximal tubules. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Kidney cells reclaim carrier-bound D3 precursor from the filtrate. organism: Mus musculus tissue_or_cell_type: kidney proximal tubule experimental_model: Mouse renal endocytosis experiments limitations: Renal endocytosis finding does not exclude free-hormone uptake elsewhere. exposure: Endogenous carrier complexes and uptake assays; timing not specified in abstract. cross_nutrient: false evidence_location: Primary abstract, receptor-mediated uptake and knockout phenotype. nutrient: Vitamin D2 and D3 [nykjaer1999] An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3. (1999). https://pubmed.ncbi.nlm.nih.gov/10052453/ DOI: 10.1016/s0092-8674(00)80655-8
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Megalin-null mice failed to retrieve filtered calcifediol and lost the vitamin D precursor in urine.

    Mouse Lrp2 gene → Urinary loss of calcifediol source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Primary abstract, receptor-mediated uptake and knockout phenotype.
    experimental_model
    Targeted megalin knockout versus controls
    exposure
    Lrp2 gene disruption; no dietary restriction inferred.
    limitations
    The knockout affects other filtered ligands too; it is machinery impairment.
    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
    Mus musculus
    plain_language
    A broken kidney uptake receptor wastes vitamin D precursor.
    primary_references
    [nykjaer1999] An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3. (1999). https://pubmed.ncbi.nlm.nih.gov/10052453/ DOI: 10.1016/s0092-8674(00)80655-8
    tissue_or_cell_type
    kidney and urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 242–255

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Targeted megalin knockout versus controls · source_derived_draft · unverified_draft

    ### vd-act-megalin-knockout-loss Megalin-null mice failed to retrieve filtered calcifediol and lost the vitamin D precursor in urine. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A broken kidney uptake receptor wastes vitamin D precursor. organism: Mus musculus tissue_or_cell_type: kidney and urine experimental_model: Targeted megalin knockout versus controls limitations: The knockout affects other filtered ligands too; it is machinery impairment. exposure: Lrp2 gene disruption; no dietary restriction inferred. cross_nutrient: false evidence_location: Primary abstract, receptor-mediated uptake and knockout phenotype. nutrient: Vitamin D2 and D3 [nykjaer1999] An endocytic pathway essential for renal uptake and activation of the steroid 25-(OH) vitamin D3. (1999). https://pubmed.ncbi.nlm.nih.gov/10052453/ DOI: 10.1016/s0092-8674(00)80655-8
    Complete structured claim and evidence

  2. Kidney cortex B12 content in megalin-deficient mice was approximately fourfold lower than in controls.

    Mouse Lrp2-null genotype → Kidney cortex cobalamin content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Megalin-deficient versus control mice
    exposure
    Genetic megalin deficiency
    limitations
    Renal content is not a universal marker of whole-body or neural B12 sufficiency; reserve function remains an interpretation.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Mus musculus
    plain_language
    Impaired renal uptake depleted the kidney B12 pool in mice.
    primary_references
    [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    tissue_or_cell_type
    Kidney cortex
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 426–437

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Megalin-deficient versus control mice · source_derived_draft · unverified_draft

    ### b12-abs-megalin-kidney-store Kidney cortex B12 content in megalin-deficient mice was approximately fourfold lower than in controls. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Impaired renal uptake depleted the kidney B12 pool in mice. organism: Mus musculus tissue_or_cell_type: Kidney cortex experimental_model: Megalin-deficient versus control mice limitations: Renal content is not a universal marker of whole-body or neural B12 sufficiency; reserve function remains an interpretation. exposure: Genetic megalin deficiency cross_nutrient: false [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    Complete structured claim and evidence

  3. Megalin-deficient mice excreted approximately fourfold more urinary B12 than controls, consistent with defective renal recovery of transcobalamin-B12.

    Mouse Lrp2-null genotype → Urinary cobalamin excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Megalin-deficient versus control mice
    exposure
    Genetic megalin deficiency
    limitations
    Mouse renal evidence; the fourfold urinary amount differs from the separately reported 28-fold clearance increase.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Mus musculus
    plain_language
    Without megalin, mice lost more B12 in urine.
    primary_references
    [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    tissue_or_cell_type
    Kidney proximal tubule/urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 413–424

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Megalin-deficient versus control mice · source_derived_draft · unverified_draft

    ### b12-abs-megalin-urinary-loss Megalin-deficient mice excreted approximately fourfold more urinary B12 than controls, consistent with defective renal recovery of transcobalamin-B12. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without megalin, mice lost more B12 in urine. organism: Mus musculus tissue_or_cell_type: Kidney proximal tubule/urine experimental_model: Megalin-deficient versus control mice limitations: Mouse renal evidence; the fourfold urinary amount differs from the separately reported 28-fold clearance increase. exposure: Genetic megalin deficiency cross_nutrient: false [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    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