Human gastric intrinsic factor / GIF

Where it participates (unsigned role)

1. In the human IF-cobalamin/CUB5-8 structure, calcium-dependent contacts connect cubilin ligand-binding domains to intrinsic factor, providing a molecular basis for calcium-dependent recognition.

   Calcium ion → Human cubilin binding of intrinsic factor-cobalamin source_derived_draftungraded
   Experimental context and source evidence

   cross_nutrient

   true

   experimental_model

   Recombinant human proteins; crystal complex at 3.3 angstrom

   exposure

   Purified complex containing calcium ions

   limitations

   Does not define a dietary calcium intake target or prove nutritional calcium deficiency causes B12 malabsorption.

   nutrient_topic

   Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)

   organism

   Homo sapiens

   plain_language

   Calcium helps intrinsic factor dock with the B12 receptor.

   primary_references

   [andersen-2010-if-cubn] Structural basis for receptor recognition of vitamin-B(12)-intrinsic factor complexes. (2010). https://pubmed.ncbi.nlm.nih.gov/20237569/ DOI: 10.1038/nature08874

   tissue_or_cell_type

   Extracellular ileal receptor binding site

   Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 257–268

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human proteins; crystal complex at 3.3 angstrom · source_derived_draft · unverified_draft

   ### b12-abs-calcium-recognition In the human IF-cobalamin/CUB5-8 structure, calcium-dependent contacts connect cubilin ligand-binding domains to intrinsic factor, providing a molecular basis for calcium-dependent recognition. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium helps intrinsic factor dock with the B12 receptor. organism: Homo sapiens tissue_or_cell_type: Extracellular ileal receptor binding site experimental_model: Recombinant human proteins; crystal complex at 3.3 angstrom limitations: Does not define a dietary calcium intake target or prove nutritional calcium deficiency causes B12 malabsorption. exposure: Purified complex containing calcium ions cross_nutrient: true [andersen-2010-if-cubn] Structural basis for receptor recognition of vitamin-B(12)-intrinsic factor complexes. (2010). https://pubmed.ncbi.nlm.nih.gov/20237569/ DOI: 10.1038/nature08874

   Complete structured claim and evidence

2. The 3.3-angstrom human IF-cobalamin/CUB5-8 structure showed two separated cubilin CUB domains engaging the two intrinsic factor domains.

   Human cubilin / CUBN → Human intrinsic factor-cobalamin complex source_derived_draftungraded
   Experimental context and source evidence

   cross_nutrient

   true

   experimental_model

   Recombinant human proteins; X-ray crystallography, PDB 3KQ4

   exposure

   Purified IF-cobalamin plus CUB5-8 fragment

   limitations

   Partial receptor crystal structure; recognition does not by itself establish endocytosis kinetics.

   nutrient_topic

   Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)

   organism

   Homo sapiens

   plain_language

   Cubilin recognizes B12 carried by intrinsic factor.

   primary_references

   [andersen-2010-if-cubn] Structural basis for receptor recognition of vitamin-B(12)-intrinsic factor complexes. (2010). https://pubmed.ncbi.nlm.nih.gov/20237569/ DOI: 10.1038/nature08874

   tissue_or_cell_type

   Extracellular ileal receptor recognition model

   Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 244–255

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human proteins; X-ray crystallography, PDB 3KQ4 · source_derived_draft · unverified_draft

   ### b12-abs-cubn-recognition The 3.3-angstrom human IF-cobalamin/CUB5-8 structure showed two separated cubilin CUB domains engaging the two intrinsic factor domains. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cubilin recognizes B12 carried by intrinsic factor. organism: Homo sapiens tissue_or_cell_type: Extracellular ileal receptor recognition model experimental_model: Recombinant human proteins; X-ray crystallography, PDB 3KQ4 limitations: Partial receptor crystal structure; recognition does not by itself establish endocytosis kinetics. exposure: Purified IF-cobalamin plus CUB5-8 fragment cross_nutrient: true [andersen-2010-if-cubn] Structural basis for receptor recognition of vitamin-B(12)-intrinsic factor complexes. (2010). https://pubmed.ncbi.nlm.nih.gov/20237569/ DOI: 10.1038/nature08874

   Complete structured claim and evidence

3. In egg-yolk transfer assays, human R binder accepted released cobalamin, whereas direct transfer to intrinsic factor was not detected and R-binder-deficient gastric juice failed to accept it.

   Human haptocorrin / TCN1 → Vitamin B12 (cobalamins) source_derived_draftungraded
   Experimental context and source evidence

   cross_nutrient

   false

   experimental_model

   In vitro egg-yolk cobalamin-binding protein mixed with human saliva/gastric juice

   exposure

   Acidified human saliva/gastric juice with egg-yolk-bound radiocobalamin

   limitations

   Food-specific biochemical model; this pH threshold is not a clinical blood threshold or proof that all foods behave identically. Pepsin preparation species was not specified in the inspected 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

   The first observed carrier was haptocorrin.

   primary_references

   [carmel-1990-food-transfer] Transfer of cobalamin from the cobalamin-binding protein of egg yolk to R binder of human saliva and gastric juice. (1990). https://pubmed.ncbi.nlm.nih.gov/2110915/ DOI: 10.1016/0016-5085(90)91076-i

   tissue_or_cell_type

   Gastric luminal digestion model

   Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 114–125

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In vitro egg-yolk cobalamin-binding protein mixed with human saliva/gastric juice · source_derived_draft · unverified_draft

   ### b12-abs-food-haptocorrin-capture In egg-yolk transfer assays, human R binder accepted released cobalamin, whereas direct transfer to intrinsic factor was not detected and R-binder-deficient gastric juice failed to accept it. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The first observed carrier was haptocorrin. organism: Homo sapiens tissue_or_cell_type: Gastric luminal digestion model experimental_model: In vitro egg-yolk cobalamin-binding protein mixed with human saliva/gastric juice limitations: Food-specific biochemical model; this pH threshold is not a clinical blood threshold or proof that all foods behave identically. Pepsin preparation species was not specified in the inspected abstract. exposure: Acidified human saliva/gastric juice with egg-yolk-bound radiocobalamin cross_nutrient: false [carmel-1990-food-transfer] Transfer of cobalamin from the cobalamin-binding protein of egg yolk to R binder of human saliva and gastric juice. (1990). https://pubmed.ncbi.nlm.nih.gov/2110915/ DOI: 10.1016/0016-5085(90)91076-i

   Complete structured claim and evidence

4. Biallelic GIF mutations in seven families with juvenile cobalamin deficiency identified inherited intrinsic-factor deficiency in cases initially suspected to have receptor-mediated IGS.

   Human biallelic GIF disease genotypes in Tanner 2005 → Intestinal cobalamin absorption source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   machinery_impairment Imported condition classification; unverified.

   cross_nutrient

   false

   experimental_model

   Human family linkage and sequencing study

   exposure

   Inherited GIF variants

   limitations

   Genetic classification; not evidence that all variants or all malabsorption have the same cause. Earlier absorption tests were inconclusive.

   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 inherited absorption failures originate in intrinsic factor.

   primary_references

   [tanner-2005-gif] Hereditary juvenile cobalamin deficiency caused by mutations in the intrinsic factor gene. (2005). https://pubmed.ncbi.nlm.nih.gov/15738392/ DOI: 10.1073/pnas.0500517102

   tissue_or_cell_type

   Gastric intrinsic factor/intestinal absorption pathway

   trigger_kind

   machinery_impairment Imported condition classification; unverified.

   Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 309–320

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family linkage and sequencing study · source_derived_draft · unverified_draft

   ### b12-abs-gif-genetic-malabsorption Biallelic GIF mutations in seven families with juvenile cobalamin deficiency identified inherited intrinsic-factor deficiency in cases initially suspected to have receptor-mediated IGS. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some inherited absorption failures originate in intrinsic factor. organism: Homo sapiens tissue_or_cell_type: Gastric intrinsic factor/intestinal absorption pathway experimental_model: Human family linkage and sequencing study limitations: Genetic classification; not evidence that all variants or all malabsorption have the same cause. Earlier absorption tests were inconclusive. exposure: Inherited GIF variants cross_nutrient: false [tanner-2005-gif] Hereditary juvenile cobalamin deficiency caused by mutations in the intrinsic factor gene. (2005). https://pubmed.ncbi.nlm.nih.gov/15738392/ DOI: 10.1073/pnas.0500517102

   Complete structured claim and evidence

5. Human salivary R protein bound cobalamin with 50-fold higher affinity than human intrinsic factor at pH 2 and threefold higher affinity at pH 8.

   Human haptocorrin / TCN1 → Vitamin B12 (cobalamins) source_derived_draftungraded
   Experimental context and source evidence

   cross_nutrient

   false

   experimental_model

   Purified human salivary R protein and gastric intrinsic factor in vitro

   exposure

   pH 2 or 8; purified protein competition

   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

   Haptocorrin outcompeted intrinsic factor, especially in acid.

   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

   Salivary/gastric and intestinal luminal binding models

   Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 153–164

   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-haptocorrin-affinity Human salivary R protein bound cobalamin with 50-fold higher affinity than human intrinsic factor at pH 2 and threefold higher affinity at pH 8. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Haptocorrin outcompeted intrinsic factor, especially in acid. organism: Homo sapiens tissue_or_cell_type: Salivary/gastric and intestinal luminal binding models 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: pH 2 or 8; purified protein competition 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

6. 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.

   Human type I intrinsic-factor blocking autoantibodies → Human intrinsic factor cobalamin-binding function source_derived_draftungraded
   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 evidence

7. Type II antibodies prevented absorption in pernicious-anemia patients when added to a preformed intrinsic-factor-B12 complex.

   Human type II intrinsic-factor binding autoantibodies → Intestinal cobalamin absorption source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   machinery_impairment Imported condition classification; unverified.

   cross_nutrient

   false

   experimental_model

   Human absorption experiments with preassembled IF-B12

   exposure

   IF plus B12 followed by type II antibody

   limitations

   Demonstrates impaired absorption; does not identify an epitope or directly prove contact competition at cubilin.

   nutrient_topic

   Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)

   organism

   Homo sapiens

   plain_language

   Other antibodies interfered even after B12 had bound its carrier.

   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

   Intestinal intrinsic-factor-dependent absorption

   trigger_kind

   machinery_impairment Imported condition classification; unverified.

   Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 517–528

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human absorption experiments with preassembled IF-B12 · source_derived_draft · unverified_draft

   ### b12-abs-if-antibody-preformed-complex Type II antibodies prevented absorption in pernicious-anemia patients when added to a preformed intrinsic-factor-B12 complex. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Other antibodies interfered even after B12 had bound its carrier. organism: Homo sapiens tissue_or_cell_type: Intestinal intrinsic-factor-dependent absorption experimental_model: Human absorption experiments with preassembled IF-B12 limitations: Demonstrates impaired absorption; does not identify an epitope or directly prove contact competition at cubilin. exposure: IF plus B12 followed by type II antibody 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 evidence

8. The pancreatic protease incubations that altered R protein did not alter the tested human intrinsic factor binding parameters.

   Pancreatic serine protease family → Human intrinsic factor cobalamin-binding function source_derived_draftungraded
   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

9. In three patients with pancreatic insufficiency, oral cobinamide 100 nmol corrected malabsorption of 0.4 nmol radiocobalamin in Schilling tests, comparably to trypsin.

   Cobinamide → Intestinal cobalamin absorption source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   machinery_impairment Imported condition classification; unverified.

   cross_nutrient

   false

   experimental_model

   Three human pancreatic-insufficiency patients and parallel human binding assays

   exposure

   Cobinamide competitor during Schilling test

   limitations

   Small physiological intervention; cobinamide is an experimental analogue, not B12 nutrition. The absorption defect was pancreatic machinery impairment.

   nutrient_topic

   Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)

   organism

   Homo sapiens

   plain_language

   Blocking haptocorrin competition restored tracer absorption in three patients.

   primary_references

   [allen-1978-cobinamide] Correction of cobalamin malabsorption in pancreatic insufficiency with a cobalamin analogue that binds with high affinity to R protein but not to intrinsic factor. In vivo evidence that a failure to partially degrade R protein is responsible for cobalamin malabsorption in pancreatic insufficiency. (1978). https://pubmed.ncbi.nlm.nih.gov/659618/ DOI: 10.1172/jci109083

   tissue_or_cell_type

   Intestinal absorption and urinary radiotracer recovery

   trigger_kind

   machinery_impairment Imported condition classification; unverified.

   Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 205–216

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three human pancreatic-insufficiency patients and parallel human binding assays · source_derived_draft · unverified_draft

   ### b12-abs-pancreatic-competitor-rescue In three patients with pancreatic insufficiency, oral cobinamide 100 nmol corrected malabsorption of 0.4 nmol radiocobalamin in Schilling tests, comparably to trypsin. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking haptocorrin competition restored tracer absorption in three patients. organism: Homo sapiens tissue_or_cell_type: Intestinal absorption and urinary radiotracer recovery experimental_model: Three human pancreatic-insufficiency patients and parallel human binding assays limitations: Small physiological intervention; cobinamide is an experimental analogue, not B12 nutrition. The absorption defect was pancreatic machinery impairment. exposure: Cobinamide competitor during Schilling test cross_nutrient: false [allen-1978-cobinamide] Correction of cobalamin malabsorption in pancreatic insufficiency with a cobalamin analogue that binds with high affinity to R protein but not to intrinsic factor. In vivo evidence that a failure to partially degrade R protein is responsible for cobalamin malabsorption in pancreatic insufficiency. (1978). https://pubmed.ncbi.nlm.nih.gov/659618/ DOI: 10.1172/jci109083

   Complete structured claim and evidence

10. Protease treatment of R-protein-bound cobalamin enabled complete transfer to human intrinsic factor within ten minutes; without proteases, transfer was not observed at pH 2 or 8.

    Pancreatic serine protease family → Cobalamin transfer from haptocorrin to human intrinsic factor source_derived_draftungraded
    Experimental context and source evidence

    cross_nutrient

    false

    experimental_model

    Purified human salivary R protein and gastric intrinsic factor in vitro

    exposure

    R protein-Cbl plus pancreatic proteases and IF

    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

    Proteolysis enabled B12 to switch carriers.

    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 179–190

    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-proteolysis-transfer Protease treatment of R-protein-bound cobalamin enabled complete transfer to human intrinsic factor within ten minutes; without proteases, transfer was not observed at pH 2 or 8. Condition category: normal nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Proteolysis enabled B12 to switch carriers. 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: R protein-Cbl plus pancreatic proteases and IF 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