Component
Mouse Abcg2 / Bcrp1
Mouse ATP-binding cassette riboflavin efflux transporter.
4 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
Intestinal ABCG2 protein increased in mangiferin-treated hyperuricemic mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"}
- experimental_model
- Rodent intestinal-loop secretion/absorption experiments
- exposure
- Mangiferin in normal and hyperuricemic loop experiments
- limitations
- Expression association does not establish direct binding; intestinal effects need not mirror kidney effects.
- nutrient_topic
- Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
- organism
- Mice for secretion/proteins; rats for absorption
- plain_language
- A shared drug and metabolite transporter changed in this tissue.
- primary_references
- [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
- tissue_or_cell_type
- Intestine
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1108–1119
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent intestinal-loop secretion/absorption experiments · source_derived_draft · unverified_draft
### mangiferin-intestinal-abcg2 Intestinal ABCG2 protein increased in mangiferin-treated hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shared drug and metabolite transporter changed in this tissue. organism: Mice for secretion/proteins; rats for absorption tissue_or_cell_type: Intestine experimental_model: Rodent intestinal-loop secretion/absorption experiments limitations: Expression association does not establish direct binding; intestinal effects need not mirror kidney effects. exposure: Mangiferin in normal and hyperuricemic loop experiments evidence_span: {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"} [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
Complete structured claim and evidence
Where it participates (unsigned role)
Curcumin increased sulfasalazine AUC about eightfold in wild-type mice but not in Bcrp-null mice.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/curcumin-research/22300367.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe", "start_char": 0, "end_char": 1713, "text_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe"}
- experimental_model
- Human pharmacokinetics, transporter vesicles and mouse knockout experiment
- exposure
- Human: curcumin 2 g before sulfasalazine 100 micrograms or 2 g; eight participants. Mouse: 300-400 mg/kg curcumin
- limitations
- Small dose- and formulation-specific drug study. Transporter inference is supported by separate assays, not a universal effect on every BCRP substrate.
- nutrient_topic
- Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
- organism
- Mus musculus
- plain_language
- Removing the transporter removed this interaction in the mouse experiment.
- primary_references
- [curcumin-p22300367] Pharmacokinetic interaction study of sulphasalazine in healthy subjects and the impact of curcumin as an in vivo inhibitor of BCRP. (2012). https://pubmed.ncbi.nlm.nih.gov/22300367/ DOI: 10.1111/j.1476-5381.2012.01887.x
- tissue_or_cell_type
- Plasma pharmacokinetics
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 814–825
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human pharmacokinetics, transporter vesicles and mouse knockout experiment · source_derived_draft · unverified_draft
### curcumin-bcrp-loss Curcumin increased sulfasalazine AUC about eightfold in wild-type mice but not in Bcrp-null mice. Condition category: machinery_impairment nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing the transporter removed this interaction in the mouse experiment. organism: Mus musculus tissue_or_cell_type: Plasma pharmacokinetics experimental_model: Human pharmacokinetics, transporter vesicles and mouse knockout experiment limitations: Small dose- and formulation-specific drug study. Transporter inference is supported by separate assays, not a universal effect on every BCRP substrate. exposure: Human: curcumin 2 g before sulfasalazine 100 micrograms or 2 g; eight participants. Mouse: 300-400 mg/kg curcumin evidence_span: {"source_cache": "artifacts/curcumin-research/22300367.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe", "start_char": 0, "end_char": 1713, "text_sha256": "a8ec64e7dff4a52838fa067fdc9418ee3ebe768c4a4d53629bd84f9f0ffe67fe"} [curcumin-p22300367] Pharmacokinetic interaction study of sulphasalazine in healthy subjects and the impact of curcumin as an in vivo inhibitor of BCRP. (2012). https://pubmed.ncbi.nlm.nih.gov/22300367/ DOI: 10.1111/j.1476-5381.2012.01887.x
Complete structured claim and evidenceMilk FAD concentrations were unchanged in Abcg2-null dams, demonstrating an ABCG2-independent route for milk vitamin B2 equivalents.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_location
- Figure 5A and discussion
- experimental_model
- Lactating knockout/wild-type mouse comparison with HPLC
- exposure
- Standard-chow lactating knockout and wild-type mice.
- limitations
- The independent FAD secretion machinery was not identified.
- nutrient_topic
- Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
- organism
- Mus musculus
- plain_language
- Milk retains another flavin supply route when free-riboflavin secretion falls.
- primary_references
- [transport-abcg2-2007] Multidrug transporter ABCG2/breast cancer resistance protein secretes riboflavin (vitamin B2) into milk. (2007). https://pmc.ncbi.nlm.nih.gov/articles/PMC1800714/ DOI: 10.1128/MCB.01621-06
- tissue_or_cell_type
- Mammary milk
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 557–568
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lactating knockout/wild-type mouse comparison with HPLC · source_derived_draft · unverified_draft
### transport-abcg2-independent-milk-fad Milk FAD concentrations were unchanged in Abcg2-null dams, demonstrating an ABCG2-independent route for milk vitamin B2 equivalents. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Milk retains another flavin supply route when free-riboflavin secretion falls. organism: Mus musculus tissue_or_cell_type: Mammary milk experimental_model: Lactating knockout/wild-type mouse comparison with HPLC limitations: The independent FAD secretion machinery was not identified. exposure: Standard-chow lactating knockout and wild-type mice. evidence_location: Figure 5A and discussion [transport-abcg2-2007] Multidrug transporter ABCG2/breast cancer resistance protein secretes riboflavin (vitamin B2) into milk. (2007). https://pmc.ncbi.nlm.nih.gov/articles/PMC1800714/ DOI: 10.1128/MCB.01621-06
Complete structured claim and evidenceAbcg2-null dams had approximately 63-fold lower free riboflavin in milk than wild type on standard chow.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_location
- Figure 5A
- experimental_model
- Lactating knockout/wild-type mouse comparison with HPLC
- exposure
- Chow containing 12-14 mg/kg riboflavin; lactating dams.
- limitations
- Mouse result; magnitude depends on chow and lactation conditions.
- nutrient_topic
- Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
- organism
- Mus musculus
- plain_language
- ABCG2 normally makes a major contribution to riboflavin delivery into milk.
- primary_references
- [transport-abcg2-2007] Multidrug transporter ABCG2/breast cancer resistance protein secretes riboflavin (vitamin B2) into milk. (2007). https://pmc.ncbi.nlm.nih.gov/articles/PMC1800714/ DOI: 10.1128/MCB.01621-06
- tissue_or_cell_type
- Mammary milk
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 544–555
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lactating knockout/wild-type mouse comparison with HPLC · source_derived_draft · unverified_draft
### transport-abcg2-milk-riboflavin Abcg2-null dams had approximately 63-fold lower free riboflavin in milk than wild type on standard chow. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: ABCG2 normally makes a major contribution to riboflavin delivery into milk. organism: Mus musculus tissue_or_cell_type: Mammary milk experimental_model: Lactating knockout/wild-type mouse comparison with HPLC limitations: Mouse result; magnitude depends on chow and lactation conditions. exposure: Chow containing 12-14 mg/kg riboflavin; lactating dams. evidence_location: Figure 5A [transport-abcg2-2007] Multidrug transporter ABCG2/breast cancer resistance protein secretes riboflavin (vitamin B2) into milk. (2007). https://pmc.ncbi.nlm.nih.gov/articles/PMC1800714/ DOI: 10.1128/MCB.01621-06
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.