Component
Neutral amino acids (assay substrates specified per claim)
Neutral amino acids (assay substrates specified per claim). Species, exposure and limitations are retained in each linked 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
SLC6A19 functioned as a sodium-dependent, chloride-independent neutral amino acid transporter.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"}
- experimental_model
- Human genetic mapping and heterologous transport-function tests
- exposure
- Hartnup-associated variants versus normal transporter
- limitations
- Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human SLC6A19
- plain_language
- Sodium coupling is also used to absorb or recover some amino acids.
- primary_references
- [sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
- tissue_or_cell_type
- Kidney/intestine transporter; expression assays
- transport_effect
- raises Sodium-dependent neutral amino acid transport, which is inward.
- transport_pool
- the expressing cell Sodium-dependent neutral amino acid transport, which is inward.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 590–601
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human genetic mapping and heterologous transport-function tests · source_derived_draft · unverified_draft
### sodium-b0at1-transport SLC6A19 functioned as a sodium-dependent, chloride-independent neutral amino acid transporter. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Sodium coupling is also used to absorb or recover some amino acids. organism: Human SLC6A19 tissue_or_cell_type: Kidney/intestine transporter; expression assays experimental_model: Human genetic mapping and heterologous transport-function tests limitations: Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage. exposure: Hartnup-associated variants versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"} [sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
Complete structured claim and evidence
Where it participates (unsigned role)
Tested Hartnup-associated SLC6A19 variants reduced neutral amino acid transport in vitro.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"}
- experimental_model
- Human genetic mapping and heterologous transport-function tests
- exposure
- Hartnup-associated variants versus normal transporter
- limitations
- Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage.
- nutrient_topic
- Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
- organism
- Human SLC6A19
- plain_language
- Even with sodium and food present, a damaged transporter can limit nutrient transport.
- primary_references
- [sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
- tissue_or_cell_type
- Kidney/intestine transporter; expression assays
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 603–614
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human genetic mapping and heterologous transport-function tests · source_derived_draft · unverified_draft
### sodium-b0at1-loss Tested Hartnup-associated SLC6A19 variants reduced neutral amino acid transport in vitro. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Even with sodium and food present, a damaged transporter can limit nutrient transport. organism: Human SLC6A19 tissue_or_cell_type: Kidney/intestine transporter; expression assays experimental_model: Human genetic mapping and heterologous transport-function tests limitations: Not every clinical feature of Hartnup disorder was explained; no direct test here of niacin supplementation or sodium shortage. exposure: Hartnup-associated variants versus normal transporter evidence_span: {"source_cache": "artifacts/sodium-research/15286788.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14", "start_char": 0, "end_char": 1040, "text_sha256": "72277489510231d6da07dacf086404f5f069094a47d7a1a2de9a8392556c3a14"} [sodium-p15286788] Hartnup disorder is caused by mutations in the gene encoding the neutral amino acid transporter SLC6A19. (2004). https://pubmed.ncbi.nlm.nih.gov/15286788/ DOI: 10.1038/ng1406
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.