Component
Human intrinsic factor cobalamin-binding function
Human intrinsic factor cobalamin-binding function
2 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.
What acts on it
Type I antibodies from pernicious-anemia sera blocked radiocobalamin binding when mixed with intrinsic factor before the vitamin, whereas prior IF-B12 formation prevented this blocking effect.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- false
- experimental_model
- Human pernicious-anemia sera; ordered-addition binding assays
- exposure
- IF plus type I antibody followed by radioactive B12 versus IF-B12 formed first
- limitations
- Sera cohort contained 79 patients; the abstract does not give functional-assay subset size. This is not every mechanism of autoimmune gastritis.
- nutrient_topic
- Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
- organism
- Homo sapiens
- plain_language
- Some antibodies stop intrinsic factor from loading B12.
- primary_references
- [schade-1967-if-antibody] Studies on antibody to intrinsic factor. (1967). https://pubmed.ncbi.nlm.nih.gov/6021209/ DOI: 10.1172/jci105563
- tissue_or_cell_type
- Human gastric intrinsic factor binding system
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 504–515
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pernicious-anemia sera; ordered-addition binding assays · source_derived_draft · unverified_draft
### b12-abs-if-antibody-blocking Type I antibodies from pernicious-anemia sera blocked radiocobalamin binding when mixed with intrinsic factor before the vitamin, whereas prior IF-B12 formation prevented this blocking effect. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some antibodies stop intrinsic factor from loading B12. organism: Homo sapiens tissue_or_cell_type: Human gastric intrinsic factor binding system experimental_model: Human pernicious-anemia sera; ordered-addition binding assays limitations: Sera cohort contained 79 patients; the abstract does not give functional-assay subset size. This is not every mechanism of autoimmune gastritis. exposure: IF plus type I antibody followed by radioactive B12 versus IF-B12 formed first cross_nutrient: false [schade-1967-if-antibody] Studies on antibody to intrinsic factor. (1967). https://pubmed.ncbi.nlm.nih.gov/6021209/ DOI: 10.1172/jci105563
Complete structured claim and evidenceThe pancreatic protease incubations that altered R protein did not alter the tested human intrinsic factor binding parameters.
Experimental context and source evidence
- cross_nutrient
- false
- experimental_model
- Purified human salivary R protein and gastric intrinsic factor in vitro
- exposure
- Parallel purified binding-protein protease incubations
- limitations
- Reconstituted binding/protease conditions; measured competition does not quantify absorption in an intact person. Individual protease isoforms and reagent species not resolved in abstract.
- nutrient_topic
- Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
- organism
- Homo sapiens
- plain_language
- Intrinsic factor retained its binding function in these assays.
- primary_references
- [allen-1978-proteases] Effect of proteolytic enzymes on the binding of cobalamin to R protein and intrinsic factor. In vitro evidence that a failure to partially degrade R protein is responsible for cobalamin malabsorption in pancreatic insufficiency. (1978). https://pubmed.ncbi.nlm.nih.gov/22556/ DOI: 10.1172/jci108924
- tissue_or_cell_type
- Duodenal luminal model
Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 192–203
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purified human salivary R protein and gastric intrinsic factor in vitro · source_derived_draft · unverified_draft
### b12-abs-if-resistance The pancreatic protease incubations that altered R protein did not alter the tested human intrinsic factor binding parameters. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Intrinsic factor retained its binding function in these assays. organism: Homo sapiens tissue_or_cell_type: Duodenal luminal model experimental_model: Purified human salivary R protein and gastric intrinsic factor in vitro limitations: Reconstituted binding/protease conditions; measured competition does not quantify absorption in an intact person. Individual protease isoforms and reagent species not resolved in abstract. exposure: Parallel purified binding-protein protease incubations cross_nutrient: false [allen-1978-proteases] Effect of proteolytic enzymes on the binding of cobalamin to R protein and intrinsic factor. In vitro evidence that a failure to partially degrade R protein is responsible for cobalamin malabsorption in pancreatic insufficiency. (1978). https://pubmed.ncbi.nlm.nih.gov/22556/ DOI: 10.1172/jci108924
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.