Component

Mouse mitochondrial aspartate aminotransferase / Got2

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.

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. Got2 knockout impaired mouse PDAC-cell growth at 0.5% oxygen more strongly than under normoxia; ETC inhibitor exposure instead exposed a distinct Got1 dependency.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse HY15549-centered CRISPR screens and knockout comparisons.
    limitations
    Do not assign all ETC-inhibitor findings to tumor hypoxia or all culture dependencies to animal tumors.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Low oxygen and a respiratory-chain drug were not identical metabolic conditions.
    primary_references
    Adaptive stimulation of macropinocytosis overcomes aspartate limitation in cancer cells under hypoxia. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35726024/ · DOI 10.1038/s42255-022-00583-z
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 242–248

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse HY15549-centered CRISPR screens and knockout comparisons. · source_derived_draft · unverified_draft

    ## l-aspartate-pdac-got2-hypoxia Low oxygen and a respiratory-chain drug were not identical metabolic conditions. Got2 knockout impaired mouse PDAC-cell growth at 0.5% oxygen more strongly than under normoxia; ETC inhibitor exposure instead exposed a distinct Got1 dependency. Model: Mouse HY15549-centered CRISPR screens and knockout comparisons. Limitations: Do not assign all ETC-inhibitor findings to tumor hypoxia or all culture dependencies to animal tumors. Evidence access: Primary full text Adaptive stimulation of macropinocytosis overcomes aspartate limitation in cancer cells under hypoxia. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35726024/ · DOI 10.1038/s42255-022-00583-z
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Isolated mouse brown-fat mitochondria reconstituted with cytosolic shuttle enzymes oxidized extramitochondrial NADH in a glutamate-dependent manner.

    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse C57BL/6J brown-fat mitochondria and reconstituted enzyme system.
    limitations
    An isolated-organelle assay does not prove that oral aspartate increases thermogenesis.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    The transport cycle linked a cytosolic redox pool to mitochondrial machinery.
    primary_references
    The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 322–328

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse C57BL/6J brown-fat mitochondria and reconstituted enzyme system. · source_derived_draft · unverified_draft

    ## l-aspartate-brown-shuttle-redox The transport cycle linked a cytosolic redox pool to mitochondrial machinery. Isolated mouse brown-fat mitochondria reconstituted with cytosolic shuttle enzymes oxidized extramitochondrial NADH in a glutamate-dependent manner. Model: Mouse C57BL/6J brown-fat mitochondria and reconstituted enzyme system. Limitations: An isolated-organelle assay does not prove that oral aspartate increases thermogenesis. Evidence access: Primary full text The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    Complete structured claim and evidence
  2. Carbon-13 glutamine tracing during mouse Listeria infection showed substantial glutamine contribution to aspartate and pyrimidine synthesis in early effector CD8 T cells.

    L-Glutamine → L-Aspartate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse in vivo tracer infusions and sorted effector T cells.
    limitations
    Fuel use changed across infection stages; no generalized human glutamine/aspartate supplementation benefit was tested.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    The immune cell used one amino acid to help supply another and build nucleotides.
    primary_references
    13C metabolite tracing reveals glutamine and acetate as critical in vivo fuels for CD8 T cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38809979/ · DOI 10.1126/sciadv.adj1431

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 274–280

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse in vivo tracer infusions and sorted effector T cells. · source_derived_draft · unverified_draft

    ## l-aspartate-tcell-glutamine-carbon The immune cell used one amino acid to help supply another and build nucleotides. Carbon-13 glutamine tracing during mouse Listeria infection showed substantial glutamine contribution to aspartate and pyrimidine synthesis in early effector CD8 T cells. Model: Mouse in vivo tracer infusions and sorted effector T cells. Limitations: Fuel use changed across infection stages; no generalized human glutamine/aspartate supplementation benefit was tested. Evidence access: Primary full text 13C metabolite tracing reveals glutamine and acetate as critical in vivo fuels for CD8 T cells. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38809979/ · DOI 10.1126/sciadv.adj1431
    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