Component

Human excitatory amino acid transporter 1 / SLC1A3

Human excitatory amino acid transporter 1 / SLC1A3

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. Increasing SLC1A3-mediated uptake supplied aspartate for nucleotide synthesis and improved proliferation under low oxygen and growth in tumor xenograft models.

    Human excitatory amino acid transporter 1 / SLC1A3 → Hypoxic proliferation of human cancer cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human cancer cultures and xenografts in immunodeficient mice.
    limitations
    Not every tumor expresses this transporter, and this is not evidence that ordinary intake initiates cancer. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Uptake partly bypassed a synthesis bottleneck in the tested tumors.
    primary_references
    Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 82–88

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer cultures and xenografts in immunodeficient mice. · source_derived_draft · unverified_draft

    ## l-aspartate-eaat1-hypoxia Uptake partly bypassed a synthesis bottleneck in the tested tumors. Increasing SLC1A3-mediated uptake supplied aspartate for nucleotide synthesis and improved proliferation under low oxygen and growth in tumor xenograft models. Model: Human cancer cultures and xenografts in immunodeficient mice. Limitations: Not every tumor expresses this transporter, and this is not evidence that ordinary intake initiates cancer. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/ Evidence access: Primary full text Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z
    Complete structured claim and evidence

  2. SLC1A3 manipulation changed aspartate import and cancer-cell sensitivity to respiratory inhibitors.

    Human excitatory amino acid transporter 1 / SLC1A3 → Resistance to ETC-inhibitor growth suppression in human cancer cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cancer-cell panels; SLC1A3 knockout/overexpression and inhibitor challenges.
    limitations
    SLC1A3 also transports glutamate; effects are model-specific rather than an oral supplementation result. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Transport capacity determines whether a cell can use the aspartate available outside it.
    primary_references
    Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 74–80

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cancer-cell panels; SLC1A3 knockout/overexpression and inhibitor challenges. · source_derived_draft · unverified_draft

    ## l-aspartate-eaat1-respiration Transport capacity determines whether a cell can use the aspartate available outside it. SLC1A3 manipulation changed aspartate import and cancer-cell sensitivity to respiratory inhibitors. Model: Human cancer-cell panels; SLC1A3 knockout/overexpression and inhibitor challenges. Limitations: SLC1A3 also transports glutamate; effects are model-specific rather than an oral supplementation result. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/ Evidence access: Primary full text Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z
    Complete structured claim and evidence

What acts on it

  1. Frontal-cortex EAAT1 protein was 62% lower in the five Wernicke cases than in five controls.

    Thiamine (vitamin B1) → Human excitatory amino acid transporter 1 / SLC1A3 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Abstract; Results; Figure 1
    evidence_span
    reduced by 62%
    experimental_model
    Human frontal-cortex autopsy samples: five male Wernicke encephalopathy cases with alcohol intake above 80 g/day versus five male controls below 20 g/day; immunoblotting and histology.
    exposure
    Neuropathologically identified Wernicke encephalopathy with heavy alcohol exposure
    limitations
    Does not isolate thiamine from alcohol effects, establish the initiating event, or directly measure uptake in living patients.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    An astrocyte glutamate transporter was reduced in the sampled diseased human cortex.
    primary_references
    [hazell-2010-human-astrocytes] Loss of astrocytic glutamate transporters in Wernicke encephalopathy (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC3388119/ DOI: 10.1002/glia.20908
    tissue_or_cell_type
    Frontal cortex
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1255–1267

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human frontal-cortex autopsy samples: five male Wernicke encephalopathy cases with alcohol intake above 80 g/day versus five male controls below 20 g/day; immunoblotting and histology. · source_derived_draft · unverified_draft

    ### thiamine-def-human-eaat1-loss Frontal-cortex EAAT1 protein was 62% lower in the five Wernicke cases than in five controls. Condition category: nutrient_deficiency nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An astrocyte glutamate transporter was reduced in the sampled diseased human cortex. organism: Homo sapiens tissue_or_cell_type: Frontal cortex experimental_model: Human frontal-cortex autopsy samples: five male Wernicke encephalopathy cases with alcohol intake above 80 g/day versus five male controls below 20 g/day; immunoblotting and histology. limitations: Does not isolate thiamine from alcohol effects, establish the initiating event, or directly measure uptake in living patients. evidence_location: Abstract; Results; Figure 1 evidence_span: reduced by 62% exposure: Neuropathologically identified Wernicke encephalopathy with heavy alcohol exposure [hazell-2010-human-astrocytes] Loss of astrocytic glutamate transporters in Wernicke encephalopathy (2010). https://pmc.ncbi.nlm.nih.gov/articles/PMC3388119/ DOI: 10.1002/glia.20908
    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