Component
Mouse vitamin D-binding protein / Gc
Mouse carrier protein used in targeted gene-disruption experiments of vitamin D transport.
3 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
Where it participates (unsigned role)
Deletion of mouse vitamin D-binding protein accelerated the loss of injected radiolabeled calcifediol from plasma.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Full primary Methods, Vitamin D kinetics; Results, kinetics of 25(OH)D3; abstract.
- experimental_model
- Radiotracer kinetics in Gc-null and wild-type mice
- exposure
- After 4-6 weeks on D3-deficient diet, 0.5 microCi or 100000 cpm tracer in homologous serum was injected intravenously; sampling over 24 h.
- limitations
- Both genotypes experienced dietary depletion; the comparison isolates an additional carrier defect. Tracer plasma residence is not a human dietary-dose trial.
- 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
- The blood carrier helps vitamin D precursor stay in circulation.
- primary_references
- [safadi1999] Osteopathy and resistance to vitamin D toxicity in mice null for vitamin D binding protein. (1999). https://pubmed.ncbi.nlm.nih.gov/9916136/ DOI: 10.1172/jci5244
- tissue_or_cell_type
- plasma and liver
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 272–285
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiotracer kinetics in Gc-null and wild-type mice · source_derived_draft · unverified_draft
### vd-act-dbp-null-retention Deletion of mouse vitamin D-binding protein accelerated the loss of injected radiolabeled calcifediol from plasma. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blood carrier helps vitamin D precursor stay in circulation. organism: Mus musculus tissue_or_cell_type: plasma and liver experimental_model: Radiotracer kinetics in Gc-null and wild-type mice limitations: Both genotypes experienced dietary depletion; the comparison isolates an additional carrier defect. Tracer plasma residence is not a human dietary-dose trial. exposure: After 4-6 weeks on D3-deficient diet, 0.5 microCi or 100000 cpm tracer in homologous serum was injected intravenously; sampling over 24 h. cross_nutrient: false evidence_location: Full primary Methods, Vitamin D kinetics; Results, kinetics of 25(OH)D3; abstract. nutrient: Vitamin D2 and D3 [safadi1999] Osteopathy and resistance to vitamin D toxicity in mice null for vitamin D binding protein. (1999). https://pubmed.ncbi.nlm.nih.gov/9916136/ DOI: 10.1172/jci5244
Complete structured claim and evidenceMegalin-null mice failed to retrieve filtered calcifediol and lost the vitamin D precursor in urine.
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 evidenceMegalin-mediated endocytosis retrieved filtered vitamin D-binding-protein/calcifediol complexes in proximal tubules.
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.