Component

Human glycine transporter 1 / SLC6A9

Context-specific entity; species, compartment and exposure are stated on each claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Human GlyT1 expressed in COS-7 cells transported glycine with sodium and chloride; the kinetic analysis used the established 2 Na+:1 Cl-:1 glycine coupling.

    Human glycine transporter 1 / SLC6A9 → Glycine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human transporter in nonhuman COS-7 host cells; whole-cell electrophysiology, usually 1 mM glycine.
    limitations
    The stoichiometry is established background incorporated into this primary kinetic study; no dietary salt intervention. Human protein and host-cell species differ.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    Glycine uptake draws on ion gradients, not just the amount of amino acid outside.
    primary_references
    A comparison of the transport kinetics of glycine transporter 1 and glycine transporter 2. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31270129/ · DOI 10.1085/jgp.201912318
    transport_effect
    raises Sodium- and chloride-coupled glycine transport, which is inward.
    transport_pool
    the expressing cell Sodium- and chloride-coupled glycine transport, which is inward.

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 26–32

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human transporter in nonhuman COS-7 host cells; whole-cell electrophysiology, usually 1 mM glycine. · source_derived_draft · unverified_draft

    ## glycine-glyt1-transport Glycine uptake draws on ion gradients, not just the amount of amino acid outside. Human GlyT1 expressed in COS-7 cells transported glycine with sodium and chloride; the kinetic analysis used the established 2 Na+:1 Cl-:1 glycine coupling. Model: Human transporter in nonhuman COS-7 host cells; whole-cell electrophysiology, usually 1 mM glycine. Limitations: The stoichiometry is established background incorporated into this primary kinetic study; no dietary salt intervention. Human protein and host-cell species differ. Evidence access: Primary full text A comparison of the transport kinetics of glycine transporter 1 and glycine transporter 2. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31270129/ · DOI 10.1085/jgp.201912318
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. GlyT1 and GlyT2 maintained forward transport under the tested elevated intracellular sodium or chloride conditions, consistent with cooperative ion/substrate binding.

    Ion/substrate coupling in human GlyT kinetic assays → Forward glycine transport in human GlyT assays source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human GlyT1/GlyT2 voltage-clamp measurements and kinetic models.
    limitations
    Binding-order models are interpretations constrained by currents, not direct structures of every transport state.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    Raising one intracellular ion did not simply switch these transporters off.
    primary_references
    A comparison of the transport kinetics of glycine transporter 1 and glycine transporter 2. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31270129/ · DOI 10.1085/jgp.201912318

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 42–48

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human GlyT1/GlyT2 voltage-clamp measurements and kinetic models. · source_derived_draft · unverified_draft

    ## glycine-glyt-ion-cooperativity Raising one intracellular ion did not simply switch these transporters off. GlyT1 and GlyT2 maintained forward transport under the tested elevated intracellular sodium or chloride conditions, consistent with cooperative ion/substrate binding. Model: Human GlyT1/GlyT2 voltage-clamp measurements and kinetic models. Limitations: Binding-order models are interpretations constrained by currents, not direct structures of every transport state. Evidence access: Primary full text A comparison of the transport kinetics of glycine transporter 1 and glycine transporter 2. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31270129/ · DOI 10.1085/jgp.201912318
    Complete structured claim and evidence

  2. Four affected individuals from two families had truncating SLC6A9 variants; two tested individuals had mildly elevated CSF glycine with normal serum glycine.

    Human truncating SLC6A9 variants → Human GLYT1 disease with CSF/serum glycine discordance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Human family sequencing and biochemical phenotyping.
    limitations
    Small rare-disease series; CSF abnormality is not inferred in untested relatives or healthy people.
    nutrient_topic
    Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Glycine
    plain_language
    A normal blood result can miss an abnormal brain-fluid pool.
    primary_references
    Loss of Glycine Transporter 1 Causes a Subtype of Glycine Encephalopathy with Arthrogryposis and Mildly Elevated Cerebrospinal Fluid Glycine. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27773429/ · DOI 10.1016/j.ajhg.2016.09.004
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Glycine: supply, one-carbon allocation, receptors and cross-nutrient mechanisms (2026-09-19) · lines 58–64

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human family sequencing and biochemical phenotyping. · source_derived_draft · unverified_draft

    ## glycine-glyt1-human-loss A normal blood result can miss an abnormal brain-fluid pool. Four affected individuals from two families had truncating SLC6A9 variants; two tested individuals had mildly elevated CSF glycine with normal serum glycine. Model: Human family sequencing and biochemical phenotyping. Limitations: Small rare-disease series; CSF abnormality is not inferred in untested relatives or healthy people. Evidence access: Primary abstract Loss of Glycine Transporter 1 Causes a Subtype of Glycine Encephalopathy with Arthrogryposis and Mildly Elevated Cerebrospinal Fluid Glycine. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27773429/ · DOI 10.1016/j.ajhg.2016.09.004
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards