Component

Mouse cytosolic aspartate aminotransferase / Got1

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

9 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. Got1 knockdown reduced glutamine-derived aspartate and impaired effector CD8 T-cell expansion in the mouse infection model.

    Mouse cytosolic aspartate aminotransferase / Got1 → Mouse effector CD8 T-cell expansion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse OT-I CD8 cells, shRNA and Listeria infection.
    limitations
    Knockdown affects related metabolic functions as well; do not attribute all outcomes only to the aspartate pool.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Internal synthesis machinery supported the expanding immune population.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 282–288

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse OT-I CD8 cells, shRNA and Listeria infection. · source_derived_draft · unverified_draft

    ## l-aspartate-tcell-got1-expansion Internal synthesis machinery supported the expanding immune population. Got1 knockdown reduced glutamine-derived aspartate and impaired effector CD8 T-cell expansion in the mouse infection model. Model: Mouse OT-I CD8 cells, shRNA and Listeria infection. Limitations: Knockdown affects related metabolic functions as well; do not attribute all outcomes only to the aspartate pool. 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

Where it participates (unsigned role)

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

    L-Glutamate → Extramitochondrial NADH oxidation in a mouse brown-fat shuttle assay source_derived_draftungraded
    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. 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.

    Mouse mitochondrial aspartate aminotransferase / Got2 → Hypoxic growth of mouse PDAC cells source_derived_draftungraded
    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

  3. 2-Oxoglutarate supplementation promoted ammonia assimilation in Got1-deficient mouse T-cell experiments, lowering the accumulated ammonia.

    2-Oxoglutarate → Ammonia accumulation in Got1-deficient mouse T cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse Got1-deficient T-cell and chronic-infection experiments.
    limitations
    Experimental rescue does not establish a human dosing strategy or replacement for intact immunity.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Supplying the nitrogen acceptor let the cells dispose of the ammonia that had built up.
    primary_references
    The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 306–312

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse Got1-deficient T-cell and chronic-infection experiments. · source_derived_draft · unverified_draft

    ## l-aspartate-tcell-akg-rescue Restoring a missing nitrogen-accepting metabolite helped recover function. 2-Oxoglutarate supplementation promoted ammonia assimilation and restored antiviral responses in Got1-deficient T-cell experiments. Model: Mouse Got1-deficient T-cell and chronic-infection experiments. Limitations: Experimental rescue does not establish a human dosing strategy or replacement for intact immunity. Evidence access: Primary abstract The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    Complete structured claim and evidence

  4. 2-Oxoglutarate supplementation promoted ammonia assimilation and restored antiviral responses in Got1-deficient T-cell experiments.

    2-Oxoglutarate → Mouse effector CD8 T-cell expansion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse Got1-deficient T-cell and chronic-infection experiments.
    limitations
    Experimental rescue does not establish a human dosing strategy or replacement for intact immunity.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Restoring a missing nitrogen-accepting metabolite helped recover function.
    primary_references
    The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 306–312

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse Got1-deficient T-cell and chronic-infection experiments. · source_derived_draft · unverified_draft

    ## l-aspartate-tcell-akg-rescue Restoring a missing nitrogen-accepting metabolite helped recover function. 2-Oxoglutarate supplementation promoted ammonia assimilation and restored antiviral responses in Got1-deficient T-cell experiments. Model: Mouse Got1-deficient T-cell and chronic-infection experiments. Limitations: Experimental rescue does not establish a human dosing strategy or replacement for intact immunity. Evidence access: Primary abstract The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    Complete structured claim and evidence

  5. Got1 deficiency lowered 2-oxoglutarate production from glutamine metabolism and caused toxic ammonia accumulation in mouse CD8 T cells during chronic infection.

    T-cell-specific Got1 loss in mice → Ammonia accumulation in Got1-deficient mouse T cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse T-cell-specific gene deletion and chronic LCMV infection.
    limitations
    This is a cell-state-specific mechanism, not a universal definition of malate–aspartate shuttle function.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    The transaminase also helped manage the nitrogen released while using glutamine.
    primary_references
    The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 298–304

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse T-cell-specific gene deletion and chronic LCMV infection. · source_derived_draft · unverified_draft

    ## l-aspartate-tcell-ammonia The transaminase also helped manage the nitrogen released while using glutamine. Got1 deficiency lowered 2-oxoglutarate production from glutamine metabolism and caused toxic ammonia accumulation in mouse CD8 T cells during chronic infection. Model: Mouse T-cell-specific gene deletion and chronic LCMV infection. Limitations: This is a cell-state-specific mechanism, not a universal definition of malate–aspartate shuttle function. Evidence access: Primary abstract The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    Complete structured claim and evidence

  6. Removing extracellular aspartate selectively reduced proliferation of Got1-silenced mouse CD8 cells, whereas control cells better tolerated its removal and viability was unchanged.

    L-Aspartate → Mouse effector CD8 T-cell expansion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse CD8 culture; Got1 knockdown with/without medium aspartate.
    limitations
    Conditional auxotrophy is not a demonstrated human dietary deficiency.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Cells depended more on external supply when synthesis was impaired.
    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
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 290–296

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse CD8 culture; Got1 knockdown with/without medium aspartate. · source_derived_draft · unverified_draft

    ## l-aspartate-tcell-external-gate Cells depended more on external supply when synthesis was impaired. Removing extracellular aspartate selectively reduced proliferation of Got1-silenced mouse CD8 cells, whereas control cells better tolerated its removal and viability was unchanged. Model: Mouse CD8 culture; Got1 knockdown with/without medium aspartate. Limitations: Conditional auxotrophy is not a demonstrated human dietary deficiency. 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

  7. 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

  8. Increasing the NAD+/NADH ratio did not restore the impaired antiviral T-cell response after Got1 loss in the tested chronic-infection setting.

    Experimental NAD+/NADH-ratio restoration in Got1-deficient T cells → Mouse effector CD8 T-cell expansion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse T-cell genetic and redox-restoration experiments.
    limitations
    Not evidence that NAD metabolism is irrelevant in other cell states.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Correcting one metabolic measurement did not fix the nitrogen-handling problem.
    primary_references
    The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 314–320

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse T-cell genetic and redox-restoration experiments. · source_derived_draft · unverified_draft

    ## l-aspartate-tcell-redox-insufficient Correcting one metabolic measurement did not fix the nitrogen-handling problem. Increasing the NAD+/NADH ratio did not restore the impaired antiviral T-cell response after Got1 loss in the tested chronic-infection setting. Model: Mouse T-cell genetic and redox-restoration experiments. Limitations: Not evidence that NAD metabolism is irrelevant in other cell states. Evidence access: Primary abstract The malate shuttle detoxifies ammonia in exhausted T cells by producing 2-ketoglutarate. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37813964/ · DOI 10.1038/s41590-023-01636-5
    Complete structured claim and evidence

In the sources

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

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