Component

Human mitochondrial aspartate aminotransferase / GOT2

Human mitochondrial aspartate aminotransferase / GOT2

4 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 acts on it

  1. Cryo-EM of human liver mitochondria resolved PLP in GOT2, with residues from both subunits forming its binding pocket.

    PLP → Human mitochondrial aspartate aminotransferase / GOT2 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human liver mitochondrial lysate cryo-EM
    limitations
    Structure demonstrates binding; it does not measure the response to B6 restriction.
    nutrient_topic
    Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
    organism
    Homo sapiens
    plain_language
    The mitochondrial aspartate enzyme also has a B6-binding catalytic site.
    primary_references
    [b6-got2-2023] High-Resolution Structural Proteomics of Mitochondria Using the 'Build and Retrieve' Methodology. (2023). https://pmc.ncbi.nlm.nih.gov/articles/PMC10709515/ DOI: 10.1016/j.mcpro.2023.100666
    tissue_or_cell_type
    Human liver mitochondrial lysate

    Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 765–774

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver mitochondrial lysate cryo-EM · source_derived_draft · unverified_draft

    ### b6-met-got2-plp Cryo-EM of human liver mitochondria resolved PLP in GOT2, with residues from both subunits forming its binding pocket. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mitochondrial aspartate enzyme also has a B6-binding catalytic site. organism: Homo sapiens tissue_or_cell_type: Human liver mitochondrial lysate experimental_model: Human liver mitochondrial lysate cryo-EM limitations: Structure demonstrates binding; it does not measure the response to B6 restriction. [b6-got2-2023] High-Resolution Structural Proteomics of Mitochondria Using the 'Build and Retrieve' Methodology. (2023). https://pmc.ncbi.nlm.nih.gov/articles/PMC10709515/ DOI: 10.1016/j.mcpro.2023.100666
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. GOT2 deletion did not reduce MIA PaCa-2 tumor size in the tested mouse xenografts, despite the synthesis dependency observed in hypoxic culture systems.

    GOT2 loss in human pancreatic cancer cells → Growth of human GOT2-null PDAC xenografts source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human MIA PaCa-2 cells implanted in mice; companion murine and PDX experiments.
    limitations
    This does not prove GOT2 is dispensable in every tumor or that it never contributes to growth.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    An animal tumor had alternative nutrient routes unavailable in the simplified culture.
    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 250–256

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human MIA PaCa-2 cells implanted in mice; companion murine and PDX experiments. · source_derived_draft · unverified_draft

    ## l-aspartate-pdac-got2-invivo-limit An animal tumor had alternative nutrient routes unavailable in the simplified culture. GOT2 deletion did not reduce MIA PaCa-2 tumor size in the tested mouse xenografts, despite the synthesis dependency observed in hypoxic culture systems. Model: Human MIA PaCa-2 cells implanted in mice; companion murine and PDX experiments. Limitations: This does not prove GOT2 is dispensable in every tumor or that it never contributes to growth. 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

  2. Increasing aspartate availability enhanced malate–aspartate shuttle use and mitochondrial metabolism of glucose-derived pyruvate in proliferating cell experiments.

    L-Aspartate → Malate–aspartate shuttle use in human proliferating cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract and primary figure descriptions
    experimental_model
    Proliferating-cell perturbation and tracer study, including human NSCLC models.
    limitations
    Substrate availability in cell models is not evidence for benefits of oral L-aspartate.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Aspartate demand for building material can compete with its participation in redox transfer.
    primary_references
    Aspartate availability drives differential engagement of the malate-aspartate shuttle. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41759528/ · DOI 10.1016/j.molcel.2026.02.004

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 226–232

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Proliferating-cell perturbation and tracer study, including human NSCLC models. · source_derived_draft · unverified_draft

    ## l-aspartate-shuttle-aspartate-availability Aspartate demand for building material can compete with its participation in redox transfer. Increasing aspartate availability enhanced malate–aspartate shuttle use and mitochondrial metabolism of glucose-derived pyruvate in proliferating cell experiments. Model: Proliferating-cell perturbation and tracer study, including human NSCLC models. Limitations: Substrate availability in cell models is not evidence for benefits of oral L-aspartate. Evidence access: Primary abstract and primary figure descriptions Aspartate availability drives differential engagement of the malate-aspartate shuttle. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41759528/ · DOI 10.1016/j.molcel.2026.02.004
    Complete structured claim and evidence

  3. Loss of shuttle components reduced pyruvate/lactate ratios and glucose-derived serine synthesis in the studied human A549 models.

    Genetic loss of shuttle components in human A549 cells → Glucose-derived serine synthesis in human A549 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract and primary figure descriptions
    experimental_model
    Human lung-cancer cell gene editing, metabolite ratios and carbon tracing.
    limitations
    A ratio is a redox proxy, and no dietary serine/aspartate deficiency threshold was measured.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Redox handling connects aspartate machinery to synthesis of another amino acid.
    primary_references
    Aspartate availability drives differential engagement of the malate-aspartate shuttle. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41759528/ · DOI 10.1016/j.molcel.2026.02.004
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 234–240

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human lung-cancer cell gene editing, metabolite ratios and carbon tracing. · source_derived_draft · unverified_draft

    ## l-aspartate-shuttle-serine-link Redox handling connects aspartate machinery to synthesis of another amino acid. Loss of shuttle components reduced pyruvate/lactate ratios and glucose-derived serine synthesis in the studied human A549 models. Model: Human lung-cancer cell gene editing, metabolite ratios and carbon tracing. Limitations: A ratio is a redox proxy, and no dietary serine/aspartate deficiency threshold was measured. Evidence access: Primary abstract and primary figure descriptions Aspartate availability drives differential engagement of the malate-aspartate shuttle. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41759528/ · DOI 10.1016/j.molcel.2026.02.004
    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