Component

GL-V9

Investigational small molecule in the 2026 colorectal-cancer study; not an approved treatment 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. GL-V9 reportedly promoted ubiquitin-proteasome degradation of DLAT.

    GL-V9 → DLAT ubiquitin-proteasome degradation source_derived_draftungraded
    Experimental context and source evidence
    access_level
    abstract_only
    compartment
    Mitochondrial GSH versus intracellular GSH distinguished by authors
    dose
    Unknown: full methods unavailable
    duration
    Unknown: full methods unavailable
    endpoint
    dlat-ubiquitin-proteasome-degradation
    evidence_location
    Primary indexed abstract; experiment-specific methods unavailable
    experimental_model
    Protein interaction/stability, knockdown and compound experiments reported in abstract
    exposure
    gl-v9
    limitations
    ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · GSH
    organism
    Human colorectal cancer models; individual experiments require full-text confirmation
    plain_language
    GL-V9 reportedly promoted ubiquitin-proteasome degradation of DLAT.
    primary_locator
    [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
    primary_references
    https://doi.org/10.1016/j.freeradbiomed.2026.04.133
    tissue_or_cell_type
    Colorectal cancer models; claim-specific cell line not established from abstract

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 886–900

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

    GL-V9 reportedly promoted ubiquitin-proteasome degradation of DLAT. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: dlat-ubiquitin-proteasome-degradation exposure: gl-v9 limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: GL-V9 reportedly promoted ubiquitin-proteasome degradation of DLAT.
    Complete structured claim and evidence

  2. GL-V9 reportedly bound DLAT.

    GL-V9 → Dihydrolipoyl acetyltransferase / DLAT source_derived_draftungraded
    Experimental context and source evidence
    access_level
    abstract_only
    compartment
    Mitochondrial GSH versus intracellular GSH distinguished by authors
    dose
    Unknown: full methods unavailable
    duration
    Unknown: full methods unavailable
    endpoint
    dlat
    evidence_location
    Primary indexed abstract; experiment-specific methods unavailable
    experimental_model
    Protein interaction/stability, knockdown and compound experiments reported in abstract
    exposure
    gl-v9
    limitations
    ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · GSH
    organism
    Human colorectal cancer models; individual experiments require full-text confirmation
    plain_language
    GL-V9 reportedly bound DLAT.
    primary_locator
    [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
    primary_references
    https://doi.org/10.1016/j.freeradbiomed.2026.04.133
    tissue_or_cell_type
    Colorectal cancer models; claim-specific cell line not established from abstract

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 869–883

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

    GL-V9 reportedly bound DLAT. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: dlat exposure: gl-v9 limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: GL-V9 reportedly bound DLAT.
    Complete structured claim and evidence

  3. GL-V9 reportedly suppressed colorectal-cancer growth in the study models.

    GL-V9 → Colorectal cancer growth in study models source_derived_draftungraded
    Experimental context and source evidence
    access_level
    abstract_only
    compartment
    Mitochondrial GSH versus intracellular GSH distinguished by authors
    dose
    Unknown: full methods unavailable
    duration
    Unknown: full methods unavailable
    endpoint
    crc-growth-model-endpoint
    evidence_location
    Primary indexed abstract; experiment-specific methods unavailable
    experimental_model
    Protein interaction/stability, knockdown and compound experiments reported in abstract
    exposure
    gl-v9
    limitations
    ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not establish model-specific dosing, safety or clinical efficacy.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · GSH
    organism
    Human colorectal cancer models; individual experiments require full-text confirmation
    plain_language
    GL-V9 reportedly suppressed colorectal-cancer growth in the study models.
    primary_locator
    [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
    primary_references
    https://doi.org/10.1016/j.freeradbiomed.2026.04.133
    tissue_or_cell_type
    Colorectal cancer models; claim-specific cell line not established from abstract

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 920–934

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

    GL-V9 reportedly suppressed colorectal-cancer growth in the study models. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: crc-growth-model-endpoint exposure: gl-v9 limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. The abstract does not establish model-specific dosing, safety or clinical efficacy. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: GL-V9 reportedly suppressed colorectal-cancer growth in the study models.
    Complete structured claim and evidence

  4. Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione.

    GL-V9 → Mammalian mitochondrial reduced-glutathione pool source_derived_draftungraded
    Experimental context and source evidence
    access_level
    abstract_only
    compartment
    Mitochondrial GSH versus intracellular GSH distinguished by authors
    dose
    Unknown: full methods unavailable
    duration
    Unknown: full methods unavailable
    endpoint
    mitochondrial-gsh-pool
    evidence_location
    Primary indexed abstract; experiment-specific methods unavailable
    experimental_model
    Protein interaction/stability, knockdown and compound experiments reported in abstract
    exposure
    gl-v9
    limitations
    ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. Abstract-reported result; specificity and rescue evidence require full text.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · GSH
    organism
    Human colorectal cancer models; individual experiments require full-text confirmation
    plain_language
    Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione.
    primary_locator
    [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}]
    primary_references
    https://doi.org/10.1016/j.freeradbiomed.2026.04.133
    tissue_or_cell_type
    Colorectal cancer models; claim-specific cell line not established from abstract

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 903–917

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Protein interaction/stability, knockdown and compound experiments reported in abstract · source_derived_draft · unverified_draft

    Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione. organism: Human colorectal cancer models; individual experiments require full-text confirmation tissue_or_cell_type: Colorectal cancer models; claim-specific cell line not established from abstract experimental_model: Protein interaction/stability, knockdown and compound experiments reported in abstract compartment: Mitochondrial GSH versus intracellular GSH distinguished by authors dose: Unknown: full methods unavailable duration: Unknown: full methods unavailable primary_references: https://doi.org/10.1016/j.freeradbiomed.2026.04.133 access_level: abstract_only evidence_location: Primary indexed abstract; experiment-specific methods unavailable endpoint: mitochondrial-gsh-pool exposure: gl-v9 limitations: ABSTRACT-ONLY CURATION. Full article and supplements were not accessible; assay-specific cell line, dose, timing, controls and sample size remain unverified. No pulmonary-endothelial or clinical-treatment inference. Abstract-reported result; specificity and rescue evidence require full text. primary_locator: [{"cache": "artifacts/dlat-curation/crc-metadata.json", "json_path": "resultList.result[0].abstractText", "access": "abstract_only"}] plain_language: Disruption of the DLAT–SLC25A39 axis by GL-V9 reportedly depleted mitochondrial glutathione.
    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