Component

Mouse EAAT3 / Slc1a1

Mouse EAAT3 / Slc1a1. Species, exposure and limitations are retained in each linked claim.

5 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. Slc1a1-null mice had lower neuronal glutathione, increased oxidant susceptibility and age-dependent brain atrophy and behavioral changes.

    Mouse EAAT3 / Slc1a1 → Mouse neuronal glutathione pool source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse EAAC1 gene deletion, hippocampal slices and aging observations.
    limitations
    Does not establish a human oral cysteine treatment or make neuronal and astrocytic transport interchangeable.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    A neuron can lack usable cysteine even when the amino acid exists elsewhere.
    primary_references
    Neuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16311588/ · DOI 10.1038/nn1609
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 100–106

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse EAAC1 gene deletion, hippocampal slices and aging observations. · source_derived_draft · unverified_draft

    ## l-cysteine-neuronal-uptake-gate A neuron can lack usable cysteine even when the amino acid exists elsewhere. Slc1a1-null mice had lower neuronal glutathione, increased oxidant susceptibility and age-dependent brain atrophy and behavioral changes. Model: Mouse EAAC1 gene deletion, hippocampal slices and aging observations. Limitations: Does not establish a human oral cysteine treatment or make neuronal and astrocytic transport interchangeable. Evidence access: Primary abstract Neuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16311588/ · DOI 10.1038/nn1609
    Complete structured claim and evidence

What acts on it

  1. The study reported increased mRNA and protein expression of the mouse intestinal transporter component SLC1A1.

    L-Theanine → Mouse EAAT3 / Slc1a1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/theanine-research/36615799.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be", "start_char": 0, "end_char": 1077, "text_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be"}
    experimental_model
    Intestinal transporter and phosphorylation assays
    exposure
    Oral L-theanine supplementation in the mouse experiment
    limitations
    Transporter expression and mTOR pathway activation were associated. Without an intervention blocking the proposed pathway, dependency is not established; no human protein-absorption benefit inferred.
    nutrient_topic
    L-Theanine research collection; topical membership is not evidence of a direct dietary effect. · L-Theanine
    organism
    Mice
    plain_language
    Each transporter remains searchable separately from the overall amino acid response.
    primary_references
    [theanine-p36615799] L-Theanine Regulates the Abundance of Amino Acid Transporters in Mice Duodenum and Jejunum via the mTOR Signaling Pathway. (2022). https://pubmed.ncbi.nlm.nih.gov/36615799/ DOI: 10.3390/nu15010142
    tissue_or_cell_type
    Intestinal amino acid transport and mTOR signaling

    L-Theanine: metabolism, neural signaling, nutrient connections and human outcomes (2026-09-17) · lines 627–638

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal transporter and phosphorylation assays · source_derived_draft · unverified_draft

    ### theanine-mouse-intestinal-slc1a1 The study reported increased mRNA and protein expression of the mouse intestinal transporter component SLC1A1. Condition category: normal nutrient_topic: L-Theanine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Each transporter remains searchable separately from the overall amino acid response. organism: Mice tissue_or_cell_type: Intestinal amino acid transport and mTOR signaling experimental_model: Intestinal transporter and phosphorylation assays limitations: Transporter expression and mTOR pathway activation were associated. Without an intervention blocking the proposed pathway, dependency is not established; no human protein-absorption benefit inferred. exposure: Oral L-theanine supplementation in the mouse experiment evidence_span: {"source_cache": "artifacts/theanine-research/36615799.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be", "start_char": 0, "end_char": 1077, "text_sha256": "0bb37e6a5f3624dc13eb87705f21721a6cf7cc2151b0ecf87dedef2ff11c95be"} [theanine-p36615799] L-Theanine Regulates the Abundance of Amino Acid Transporters in Mice Duodenum and Jejunum via the mTOR Signaling Pathway. (2022). https://pubmed.ncbi.nlm.nih.gov/36615799/ DOI: 10.3390/nu15010142
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. N-acetylcysteine treatment reversed reduced neuronal glutathione and oxidant-related abnormalities in EAAC1-deficient mice.

    N-Acetyl-L-cysteine → Mouse neuronal glutathione pool source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse Slc1a1 deletion with NAC treatment.
    limitations
    NAC is the tested intervention, not free L-cysteine; no human cognitive benefit is established.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    A different precursor bypassed part of the uptake limitation in this animal model.
    primary_references
    Neuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16311588/ · DOI 10.1038/nn1609
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 108–114

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse Slc1a1 deletion with NAC treatment. · source_derived_draft · unverified_draft

    ## l-cysteine-nac-neuronal-rescue A different precursor bypassed part of the uptake limitation in this animal model. N-acetylcysteine treatment reversed reduced neuronal glutathione and oxidant-related abnormalities in EAAC1-deficient mice. Model: Mouse Slc1a1 deletion with NAC treatment. Limitations: NAC is the tested intervention, not free L-cysteine; no human cognitive benefit is established. Evidence access: Primary abstract Neuronal glutathione deficiency and age-dependent neurodegeneration in the EAAC1 deficient mouse. · 2006 · https://pubmed.ncbi.nlm.nih.gov/16311588/ · DOI 10.1038/nn1609
    Complete structured claim and evidence

  2. EAAC1-null mice had increased vesicular/cytosolic hippocampal zinc and greater zinc redistribution and neuronal injury after transient cerebral ischemia.

    Mouse EAAC1 loss → Labile zinc in mouse hippocampal neurons source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse knockout, zinc measurements and transient ischemia.
    limitations
    The experiment did not test dietary zinc deficiency or toxicity thresholds.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Impaired cysteine supply affected metal handling as well as antioxidant capacity.
    primary_references
    EAAC1 gene deletion alters zinc homeostasis and exacerbates neuronal injury after transient cerebral ischemia. · 2010 · https://pubmed.ncbi.nlm.nih.gov/21084597/ · DOI 10.1523/JNEUROSCI.2084-10.2010
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 116–122

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse knockout, zinc measurements and transient ischemia. · source_derived_draft · unverified_draft

    ## l-cysteine-neuronal-zinc-link Impaired cysteine supply affected metal handling as well as antioxidant capacity. EAAC1-null mice had increased vesicular/cytosolic hippocampal zinc and greater zinc redistribution and neuronal injury after transient cerebral ischemia. Model: Mouse knockout, zinc measurements and transient ischemia. Limitations: The experiment did not test dietary zinc deficiency or toxicity thresholds. Evidence access: Primary abstract EAAC1 gene deletion alters zinc homeostasis and exacerbates neuronal injury after transient cerebral ischemia. · 2010 · https://pubmed.ncbi.nlm.nih.gov/21084597/ · DOI 10.1523/JNEUROSCI.2084-10.2010
    Complete structured claim and evidence

  3. NAC restored neuronal glutathione and normalized basal zinc levels in EAAC1-null mice; NAC or zinc chelation reduced ischemia-associated zinc movement, superoxide and neuronal death.

    N-Acetyl-L-cysteine → Labile zinc in mouse hippocampal neurons source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse EAAC1-null ischemia model.
    limitations
    NAC and chelators are separate interventions; the study does not show that extra dietary cysteine and zinc are synergistic.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Restoring precursor supply and binding excess labile zinc were distinct rescue routes.
    primary_references
    EAAC1 gene deletion alters zinc homeostasis and exacerbates neuronal injury after transient cerebral ischemia. · 2010 · https://pubmed.ncbi.nlm.nih.gov/21084597/ · DOI 10.1523/JNEUROSCI.2084-10.2010
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 124–130

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse EAAC1-null ischemia model. · source_derived_draft · unverified_draft

    ## l-cysteine-neuronal-zinc-rescue Restoring precursor supply and binding excess labile zinc were distinct rescue routes. NAC restored neuronal glutathione and normalized basal zinc levels in EAAC1-null mice; NAC or zinc chelation reduced ischemia-associated zinc movement, superoxide and neuronal death. Model: Mouse EAAC1-null ischemia model. Limitations: NAC and chelators are separate interventions; the study does not show that extra dietary cysteine and zinc are synergistic. Evidence access: Primary abstract EAAC1 gene deletion alters zinc homeostasis and exacerbates neuronal injury after transient cerebral ischemia. · 2010 · https://pubmed.ncbi.nlm.nih.gov/21084597/ · DOI 10.1523/JNEUROSCI.2084-10.2010
    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