Component
b0,+AT-rBAT complex
Independent protein complex record; interpretation is limited by each linked claim and its study context.
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.
What it acts on
SLC7A9 associated with SLC3A1 mediates sodium-independent lysine exchange at the apical epithelial membrane.
Experimental context and source evidence
- experimental_model
- Human/mouse cloning, Xenopus transport and renal localization
- limitations
- Leucine is an example exchange substrate, not the obligatory unique counter-substrate.
- organism
- Human and mouse proteins; Xenopus expression system
- plain_language
- This transporter admits lysine at the gut or kidney lumen-facing surface.
- primary_references
- [pfeiffer1999b0] Luminal Heterodimeric Amino Acid Transporter Defective in Cystinuria (1999). https://pmc.ncbi.nlm.nih.gov/articles/PMC25748/ DOI: 10.1091/mbc.10.12.4135
- tissue_or_cell_type
- Renal proximal-tubule brush border; intestinal apical context
- transport_effect
- depends The record names sodium-independent lysine exchange and not which way lysine moves in it.
- transport_pool
- the enterocyte interior across the apical membrane The record names sodium-independent lysine exchange and not which way lysine moves in it.
L-Lysine: mechanism-first literature curation (2026-09-17) · lines 24–32
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human/mouse cloning, Xenopus transport and renal localization · source_derived_draft · unverified_draft
### apical-lysine-exchange SLC7A9 associated with SLC3A1 mediates sodium-independent lysine exchange at the apical epithelial membrane. Plain language: This transporter admits lysine at the gut or kidney lumen-facing surface. Condition category: normal organism: Human and mouse proteins; Xenopus expression system tissue_or_cell_type: Renal proximal-tubule brush border; intestinal apical context experimental_model: Human/mouse cloning, Xenopus transport and renal localization limitations: Leucine is an example exchange substrate, not the obligatory unique counter-substrate. [pfeiffer1999b0] Luminal Heterodimeric Amino Acid Transporter Defective in Cystinuria (1999). https://pmc.ncbi.nlm.nih.gov/articles/PMC25748/ DOI: 10.1091/mbc.10.12.4135
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.