Component
Human proton-coupled amino acid transporter 2 / SLC36A2
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 it acts on
Inheritance and functional studies in seven families implicated nonfunctional SLC36A2 alleles in urinary glycine and imino-acid loss; two defective alleles tracked iminoglycinuria and one tracked hyperglycinuria.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human family genetics with functional transporter testing.
- limitations
- This is renal handling; urinary loss alone does not establish systemic nutritional deficiency.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- The kidney can lose glycine because its recovery transporter is faulty.
- primary_references
- Iminoglycinuria and hyperglycinuria are discrete human phenotypes resulting from complex mutations in proline and glycine transporters. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19033659/ · DOI 10.1172/JCI36625
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 66–72
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human family genetics with functional transporter testing. · source_derived_draft · unverified_draft
## glycine-renal-pat2 The kidney can lose glycine because its recovery transporter is faulty. Inheritance and functional studies in seven families implicated nonfunctional SLC36A2 alleles in urinary glycine and imino-acid loss; two defective alleles tracked iminoglycinuria and one tracked hyperglycinuria. Model: Human family genetics with functional transporter testing. Limitations: This is renal handling; urinary loss alone does not establish systemic nutritional deficiency. Evidence access: Primary abstract Iminoglycinuria and hyperglycinuria are discrete human phenotypes resulting from complex mutations in proline and glycine transporters. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19033659/ · DOI 10.1172/JCI36625
Complete structured claim and evidence
Where it participates (unsigned role)
SLC6A20 mutations accompanied iminoglycinuria when combined with SLC36A2 variants retaining residual transport.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Human family genotype/functional analysis.
- limitations
- Modifier evidence is not proof of ordinary dietary competition between glycine and proline.
- nutrient_topic
- Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
- plain_language
- A second transporter can change the effect of the first defect.
- primary_references
- Iminoglycinuria and hyperglycinuria are discrete human phenotypes resulting from complex mutations in proline and glycine transporters. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19033659/ · DOI 10.1172/JCI36625
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 74–80
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human family genotype/functional analysis. · source_derived_draft · unverified_draft
## glycine-renal-modifier A second transporter can change the effect of the first defect. SLC6A20 mutations accompanied iminoglycinuria when combined with SLC36A2 variants retaining residual transport. Model: Human family genotype/functional analysis. Limitations: Modifier evidence is not proof of ordinary dietary competition between glycine and proline. Evidence access: Primary abstract Iminoglycinuria and hyperglycinuria are discrete human phenotypes resulting from complex mutations in proline and glycine transporters. · 2008 · https://pubmed.ncbi.nlm.nih.gov/19033659/ · DOI 10.1172/JCI36625
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.