Component

Human glutaminase 2 / GLS2

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

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 it acts on

  1. GLS2 manipulation linked increased glutamate and 2-oxoglutarate production with increased respiration and ATP generation in the tested human cells.

    Human glutaminase 2 / GLS2 → Respiration and ATP production in human GLS2 experiments source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human-cell GLS2 expression/perturbation study.
    limitations
    The effect depends on cell context; it is not a clinical energy claim.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    The generated carbon skeleton can support mitochondrial metabolism.
    primary_references
    Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 218–224

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human-cell GLS2 expression/perturbation study. · source_derived_draft · unverified_draft

    ## glutamate-gls2-energy The generated carbon skeleton can support mitochondrial metabolism. GLS2 manipulation linked increased glutamate and 2-oxoglutarate production with increased respiration and ATP generation in the tested human cells. Model: Human-cell GLS2 expression/perturbation study. Limitations: The effect depends on cell context; it is not a clinical energy claim. Evidence access: Primary abstract Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107
    Complete structured claim and evidence

  2. Increasing GLS2 supported higher reduced-glutathione levels, lower reactive oxygen species and protection from peroxide-induced apoptosis in the reported cell experiments.

    Human glutaminase 2 / GLS2 → GSH source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human-cell GLS2/p53 and oxidative-stress experiments.
    limitations
    Cysteine, glycine and synthesis machinery remain necessary; glutamate is not established as the universal limiting substrate.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    The same supply route fed antioxidant chemistry as well as energy metabolism.
    primary_references
    Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling 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 · Human-cell GLS2/p53 and oxidative-stress experiments. · source_derived_draft · unverified_draft

    ## glutamate-gls2-gsh The same supply route fed antioxidant chemistry as well as energy metabolism. Increasing GLS2 supported higher reduced-glutathione levels, lower reactive oxygen species and protection from peroxide-induced apoptosis in the reported cell experiments. Model: Human-cell GLS2/p53 and oxidative-stress experiments. Limitations: Cysteine, glycine and synthesis machinery remain necessary; glutamate is not established as the universal limiting substrate. Evidence access: Primary abstract Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107
    Complete structured claim and evidence

  3. The primary study identifies GLS2 as a mitochondrial glutaminase hydrolyzing glutamine to glutamate.

    Human glutaminase 2 / GLS2 → L-Glutamate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human-cell GLS2/p53 study; reaction identity described alongside functional experiments.
    limitations
    GLS2 and the distinct GLS gene are not interchangeable.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    A related amino acid is an upstream source of glutamate.
    primary_references
    Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 202–208

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human-cell GLS2/p53 study; reaction identity described alongside functional experiments. · source_derived_draft · unverified_draft

    ## glutamate-gls2-production A related amino acid is an upstream source of glutamate. The primary study identifies GLS2 as a mitochondrial glutaminase hydrolyzing glutamine to glutamate. Model: Human-cell GLS2/p53 study; reaction identity described alongside functional experiments. Limitations: GLS2 and the distinct GLS gene are not interchangeable. Evidence access: Primary abstract Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107
    Complete structured claim and evidence

What acts on it

  1. Activating p53 increased GLS2 expression under stressed and unstressed conditions in the reported human-cell experiments.

    Human tumor protein p53 / TP53 → Human glutaminase 2 / GLS2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human-cell p53 and GLS2 expression/perturbation assays.
    limitations
    A tumor-suppressor pathway is not evidence that glutamate supplementation prevents cancer.
    nutrient_topic
    L-Glutamate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Glutamate
    plain_language
    Gene regulation changes the machinery that supplies glutamate.
    primary_references
    Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107

    L-Glutamate / L-glutamic acid: carbon and nitrogen allocation, signaling and cross-nutrient mechanisms (2026-09-19) · lines 210–216

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human-cell p53 and GLS2 expression/perturbation assays. · source_derived_draft · unverified_draft

    ## glutamate-p53-gls2 Gene regulation changes the machinery that supplies glutamate. Activating p53 increased GLS2 expression under stressed and unstressed conditions in the reported human-cell experiments. Model: Human-cell p53 and GLS2 expression/perturbation assays. Limitations: A tumor-suppressor pathway is not evidence that glutamate supplementation prevents cancer. Evidence access: Primary abstract Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20378837/ · DOI 10.1073/pnas.1001006107
    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