Component
Mouse intestinal tryptophan uptake
Context-specific entity; species, compartment and exposure are stated on each claim.
1 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.
Where it participates (unsigned role)
Ace2 loss removed intestinal B0AT1 expression in mice; kidney B0AT1 regulation differed and depended on collectrin.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text, partner constructs and mouse tissue results
- experimental_model
- Mouse tissue expression and transporter-partner experiments.
- limitations
- Separate oocyte experiments combine human B0AT1 with mouse ACE2 or human collectrin; they are not an all-human ACE2 reconstruction.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- The same amino-acid transporter needs different support in intestine and kidney.
- 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.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 66–72
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse tissue expression and transporter-partner experiments. · source_derived_draft · unverified_draft
## tryptophan-ace2-transporter The same amino-acid transporter needs different support in intestine and kidney. Ace2 loss removed intestinal B0AT1 expression in mice; kidney B0AT1 regulation differed and depended on collectrin. Model: Mouse tissue expression and transporter-partner experiments. Limitations: Separate oocyte experiments combine human B0AT1 with mouse ACE2 or human collectrin; they are not an all-human ACE2 reconstruction. Evidence access: Primary full text, partner constructs and mouse tissue results 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.