Component
Mouse sodium/imino-acid transporter / Slc6a20a
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
Mice carrying C-terminally truncated PTEN showed increased Slc6a20a expression, lower extracellular brain proline and glycine, and reduced NMDAR currents.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Engineered mouse PTEN model; transcriptional, microdialysis and electrophysiological observations.
- limitations
- Multiple consequences of PTEN mutation remain possible; the model is not ordinary dietary deficiency. Correction record: Author correction PMID 39242973 / DOI 10.1038/s44321-024-00125-y corrects the human embryonic stem-cell neuron protocol IRB approval number to KH2017-109 from KA2018-61 and KH2020-55. It does not report a change to experimental results. https://link.springer.com/article/10.1038/s44321-024-00125-y
- nutrient_topic
- L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
- plain_language
- Transporter regulation can alter the extracellular supply of two amino acids together.
- primary_references
- SLC6A20 transporter: a novel regulator of brain glycine homeostasis and NMDAR function. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33428810/ · DOI 10.15252/emmm.202012632
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Proline: synthesis, collagen processing, redox metabolism and cross-nutrient mechanisms (2026-09-19) · lines 214–220
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Engineered mouse PTEN model; transcriptional, microdialysis and electrophysiological observations. · source_derived_draft · unverified_draft
## l-proline-brain-transporter-increase Transporter regulation can alter the extracellular supply of two amino acids together. Mice carrying C-terminally truncated PTEN showed increased Slc6a20a expression, lower extracellular brain proline and glycine, and reduced NMDAR currents. Model: Engineered mouse PTEN model; transcriptional, microdialysis and electrophysiological observations. Limitations: Multiple consequences of PTEN mutation remain possible; the model is not ordinary dietary deficiency. Correction record: Author correction PMID 39242973 / DOI 10.1038/s44321-024-00125-y corrects the human embryonic stem-cell neuron protocol IRB approval number to KH2017-109 from KA2018-61 and KH2020-55. It does not report a change to experimental results. https://link.springer.com/article/10.1038/s44321-024-00125-y Evidence access: Primary full text SLC6A20 transporter: a novel regulator of brain glycine homeostasis and NMDAR function. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33428810/ · DOI 10.15252/emmm.202012632
Complete structured claim and evidenceSlc6a20a-knockout mice had higher extracellular brain glycine and increased NMDA-receptor currents.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Mouse genetic deletion with extracellular amino-acid measurements and electrophysiology.
- limitations
- This does not show that oral proline treats NMDAR dysfunction in humans. Correction record: Author correction PMID 39242973 / DOI 10.1038/s44321-024-00125-y corrects the human embryonic stem-cell neuron protocol IRB approval number to KH2017-109 from KA2018-61 and KH2020-55. It does not report a change to experimental results. https://link.springer.com/article/10.1038/s44321-024-00125-y
- nutrient_topic
- L-Proline collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Proline
- plain_language
- Changing a proline-sharing transporter can change glycine-dependent brain signaling.
- primary_references
- SLC6A20 transporter: a novel regulator of brain glycine homeostasis and NMDAR function. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33428810/ · DOI 10.15252/emmm.202012632
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Proline: synthesis, collagen processing, redox metabolism and cross-nutrient mechanisms (2026-09-19) · lines 206–212
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic deletion with extracellular amino-acid measurements and electrophysiology. · source_derived_draft · unverified_draft
## l-proline-brain-transporter-loss Changing a proline-sharing transporter can change glycine-dependent brain signaling. Slc6a20a-knockout mice had higher extracellular brain glycine and increased NMDA-receptor currents. Model: Mouse genetic deletion with extracellular amino-acid measurements and electrophysiology. Limitations: This does not show that oral proline treats NMDAR dysfunction in humans. Correction record: Author correction PMID 39242973 / DOI 10.1038/s44321-024-00125-y corrects the human embryonic stem-cell neuron protocol IRB approval number to KH2017-109 from KA2018-61 and KH2020-55. It does not report a change to experimental results. https://link.springer.com/article/10.1038/s44321-024-00125-y Evidence access: Primary full text SLC6A20 transporter: a novel regulator of brain glycine homeostasis and NMDAR function. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33428810/ · DOI 10.15252/emmm.202012632
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.