Component
Isoleucine uptake in mouse ileum
Context-specific entity; species, compartment and exposure are stated on each claim.
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
Ace2 deletion removed intestinal B0AT1 expression and abolished sodium-dependent isoleucine uptake in mouse ileum segments.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Ace2-null mouse intestine; expression, interaction and uptake assays.
- limitations
- Kidney accessory-protein dependence differs; not evidence that every change in ACE2 produces dietary isoleucine deficiency.
- nutrient_topic
- L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
- plain_language
- A working transporter also needs its accessory protein in this tissue.
- primary_references
- Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 26–32
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Ace2-null mouse intestine; expression, interaction and uptake assays. · source_derived_draft · unverified_draft
## isoleucine-intestinal-ace2 A working transporter also needs its accessory protein in this tissue. Ace2 deletion removed intestinal B0AT1 expression and abolished sodium-dependent isoleucine uptake in mouse ileum segments. Model: Ace2-null mouse intestine; expression, interaction and uptake assays. Limitations: Kidney accessory-protein dependence differs; not evidence that every change in ACE2 produces dietary isoleucine deficiency. Evidence access: Primary full text Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
Complete structured claim and evidenceReplacing sodium during mouse ileum uptake assays removed the sodium-dependent component of radiolabeled L-isoleucine uptake.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Everted mouse ileum; 1 mM L-isoleucine, five-minute uptake assay.
- limitations
- Does not imply extra dietary sodium improves absorption in sodium-replete people.
- nutrient_topic
- L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
- plain_language
- An ion gradient helps the intestine take up this amino acid.
- primary_references
- Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 18–24
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Everted mouse ileum; 1 mM L-isoleucine, five-minute uptake assay. · source_derived_draft · unverified_draft
## isoleucine-intestinal-sodium An ion gradient helps the intestine take up this amino acid. Replacing sodium during mouse ileum uptake assays removed the sodium-dependent component of radiolabeled L-isoleucine uptake. Model: Everted mouse ileum; 1 mM L-isoleucine, five-minute uptake assay. Limitations: Does not imply extra dietary sodium improves absorption in sodium-replete people. Evidence access: Primary full text Tissue-specific amino acid transporter partners ACE2 and collectrin differentially interact with hartnup mutations. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19185582/ · DOI 10.1053/j.gastro.2008.10.055
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.