Component
Intestine-specific homeobox protein / ISX
Independent protein identity; organism and experimental state are specified on individual claims.
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 it acts on
ISX recognized upstream BCO1 regulatory motifs and repressed its expression.
Experimental context and source evidence
- evidence_location
- Abstract
- experimental_model
- Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets.
- exposure
- ISX binding and gene-expression experiments.
- limitations
- Does not establish a fixed carotenoid conversion ratio.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus and promoter-binding preparations
- outcome
- ISX recognized upstream BCO1 regulatory motifs and repressed its expression.
- plain_language
- The same feedback factor limits the carotenoid-cleaving enzyme.
- primary_references
- [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
- tissue_or_cell_type
- Intestinal epithelium
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 288–300
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. · source_derived_draft · unverified_draft
### va-isx-bco1-repression ISX recognized upstream BCO1 regulatory motifs and repressed its expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same feedback factor limits the carotenoid-cleaving enzyme. organism: Mus musculus and promoter-binding preparations tissue_or_cell_type: Intestinal epithelium experimental_model: Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. limitations: Does not establish a fixed carotenoid conversion ratio. exposure: ISX binding and gene-expression experiments. outcome: ISX recognized upstream BCO1 regulatory motifs and repressed its expression. evidence_location: Abstract [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
Complete structured claim and evidenceIsx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Retinoid/ISX control of a shared intestinal transporter affects vitamin E status.
- evidence_location
- Figure 7
- experimental_model
- Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets.
- exposure
- Females; ten weeks of AIN93G with 75 IU vitamin E/kg, with or without 50 mg zeaxanthin/kg.
- limitations
- Accumulation is not a clinical benefit; compound mutants had a larger effect than Isx single mutants.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus
- outcome
- Isx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels.
- plain_language
- Disrupting vitamin A feedback also changed vitamin E accumulation.
- primary_references
- [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
- tissue_or_cell_type
- Jejunum and liver
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 302–315
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. · source_derived_draft · unverified_draft
### va-isx-loss-tocopherol Isx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Disrupting vitamin A feedback also changed vitamin E accumulation. organism: Mus musculus tissue_or_cell_type: Jejunum and liver experimental_model: Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. limitations: Accumulation is not a clinical benefit; compound mutants had a larger effect than Isx single mutants. exposure: Females; ten weeks of AIN93G with 75 IU vitamin E/kg, with or without 50 mg zeaxanthin/kg. outcome: Isx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels. evidence_location: Figure 7 cross_nutrient: Retinoid/ISX control of a shared intestinal transporter affects vitamin E status. [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
Complete structured claim and evidenceISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.
Experimental context and source evidence
- evidence_location
- Abstract
- experimental_model
- Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets.
- exposure
- Isx genotypes and promoter-binding experiments.
- limitations
- Tissue-specific regulation, not suppression in every organ.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus and promoter-binding preparations
- outcome
- ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.
- plain_language
- The feedback factor lowers the uptake receptor.
- primary_references
- [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
- tissue_or_cell_type
- Jejunum and DNA-binding assays
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 274–286
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. · source_derived_draft · unverified_draft
### va-isx-scarb1-repression ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The feedback factor lowers the uptake receptor. organism: Mus musculus and promoter-binding preparations tissue_or_cell_type: Jejunum and DNA-binding assays experimental_model: Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. limitations: Tissue-specific regulation, not suppression in every organ. exposure: Isx genotypes and promoter-binding experiments. outcome: ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. evidence_location: Abstract [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
Complete structured claim and evidence
What acts on it
Retinoic-acid receptor signaling increased intestinal ISX expression.
Experimental context and source evidence
- evidence_location
- Abstract
- experimental_model
- Mouse diet/retinoic-acid interventions and human cell lines.
- exposure
- Retinoic-acid treatment with receptor-dependent tests.
- limitations
- Pharmacological treatment supports feedback circuitry, not a universal dietary threshold.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus and Homo sapiens cell lines
- outcome
- Retinoic-acid receptor signaling increased intestinal ISX expression.
- plain_language
- The active retinoid metabolite induces a brake on further precursor uptake.
- primary_references
- [va-lobo-2010] ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production (2010). https://pubmed.ncbi.nlm.nih.gov/20061533/ DOI: 10.1096/fj.09-150995
- tissue_or_cell_type
- Intestine and cultured cells
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 260–272
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse diet/retinoic-acid interventions and human cell lines. · source_derived_draft · unverified_draft
### va-retinoic-acid-isx-feedback Retinoic-acid receptor signaling increased intestinal ISX expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The active retinoid metabolite induces a brake on further precursor uptake. organism: Mus musculus and Homo sapiens cell lines tissue_or_cell_type: Intestine and cultured cells experimental_model: Mouse diet/retinoic-acid interventions and human cell lines. limitations: Pharmacological treatment supports feedback circuitry, not a universal dietary threshold. exposure: Retinoic-acid treatment with receptor-dependent tests. outcome: Retinoic-acid receptor signaling increased intestinal ISX expression. evidence_location: Abstract [va-lobo-2010] ISX is a retinoic acid-sensitive gatekeeper that controls intestinal beta,beta-carotene absorption and vitamin A production (2010). https://pubmed.ncbi.nlm.nih.gov/20061533/ DOI: 10.1096/fj.09-150995
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.