Component

SLC25A39-knockout mammalian cells

SLC25A39-knockout mammalian cells. Species, exposure and limitations are retained in each linked 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. Whole-cell GSH levels were not reduced by SLC25A39 loss.

    SLC25A39-knockout mammalian cells → Cellular reduced-glutathione pool source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"}
    experimental_model
    Organelle metabolomics, genetics and targeted synthesis rescue
    exposure
    SLC25A39 loss, A39/A40 double loss and targeted GshF
    limitations
    Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Mammalian cells; separate mouse erythropoiesis experiments
    plain_language
    A normal total-cell result could conceal a mitochondrial shortage.
    primary_references
    [glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w
    tissue_or_cell_type
    Mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 476–487

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Organelle metabolomics, genetics and targeted synthesis rescue · source_derived_draft · unverified_draft

    ### glutathione-a39-cellular-null Whole-cell GSH levels were not reduced by SLC25A39 loss. Condition category: machinery_impairment nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: A normal total-cell result could conceal a mitochondrial shortage. organism: Mammalian cells; separate mouse erythropoiesis experiments tissue_or_cell_type: Mitochondria experimental_model: Organelle metabolomics, genetics and targeted synthesis rescue limitations: Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation. exposure: SLC25A39 loss, A39/A40 double loss and targeted GshF evidence_span: {"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"} [glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w
    Complete structured claim and evidence

  2. SLC25A39 loss reduced mitochondrial GSH abundance.

    SLC25A39-knockout mammalian cells → Mammalian mitochondrial reduced-glutathione pool source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"}
    experimental_model
    Organelle metabolomics, genetics and targeted synthesis rescue
    exposure
    SLC25A39 loss, A39/A40 double loss and targeted GshF
    limitations
    Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Mammalian cells; separate mouse erythropoiesis experiments
    plain_language
    The affected compartment lost its supply.
    primary_references
    [glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w
    tissue_or_cell_type
    Mitochondria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 463–474

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Organelle metabolomics, genetics and targeted synthesis rescue · source_derived_draft · unverified_draft

    ### glutathione-a39-pool SLC25A39 loss reduced mitochondrial GSH abundance. Condition category: machinery_impairment nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: The affected compartment lost its supply. organism: Mammalian cells; separate mouse erythropoiesis experiments tissue_or_cell_type: Mitochondria experimental_model: Organelle metabolomics, genetics and targeted synthesis rescue limitations: Mitochondrial versus total-cell pools differ; engineered synthesis rescue is not oral supplementation. exposure: SLC25A39 loss, A39/A40 double loss and targeted GshF evidence_span: {"source_cache": "artifacts/glutathione-research/34707288.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5", "start_char": 0, "end_char": 1450, "text_sha256": "7e6a64f24da95b93d7440f3424bb8a611f3fc962a5dd6344f5d0e11671e0bba5"} [glutathione-p34707288] SLC25A39 is necessary for mitochondrial glutathione import in mammalian cells. (2021). https://pubmed.ncbi.nlm.nih.gov/34707288/ DOI: 10.1038/s41586-021-04025-w
    Complete structured claim and evidence

  3. A39 loss impaired early metastatic colonization in the tested breast-cancer models.

    SLC25A39-knockout mammalian cells → Early lung colonization in SLC25A39-dependent breast-cancer models source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"}
    experimental_model
    Genetic screens, cancer models and patient-derived xenografts
    exposure
    SLC25A39 loss and ATF4 CRISPR activation
    limitations
    Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Experimental breast-cancer cells and mouse xenografts
    plain_language
    Glutathione-dependent machinery can also support an unwanted cell process.
    primary_references
    [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    tissue_or_cell_type
    Early lung metastatic colonization

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 1321–1332

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screens, cancer models and patient-derived xenografts · source_derived_draft · unverified_draft

    ### glutathione-metastasis-a39 A39 loss impaired early metastatic colonization in the tested breast-cancer models. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Glutathione-dependent machinery can also support an unwanted cell process. organism: Experimental breast-cancer cells and mouse xenografts tissue_or_cell_type: Early lung metastatic colonization experimental_model: Genetic screens, cancer models and patient-derived xenografts limitations: Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people. exposure: SLC25A39 loss and ATF4 CRISPR activation evidence_span: {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"} [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    Complete structured claim and evidence

  4. Primary tumor growth was unaffected by A39 loss in the reported comparison.

    SLC25A39-knockout mammalian cells → Primary tumor growth in the SLC25A39 breast-cancer study source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"}
    experimental_model
    Genetic screens, cancer models and patient-derived xenografts
    exposure
    SLC25A39 loss and ATF4 CRISPR activation
    limitations
    Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people.
    nutrient_topic
    Glutathione research collection; topical membership is not evidence of a direct dietary effect. · GSH
    organism
    Experimental breast-cancer cells and mouse xenografts
    plain_language
    Early colonization and growth of the original tumor were distinct endpoints.
    primary_references
    [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    tissue_or_cell_type
    Early lung metastatic colonization

    Glutathione: metabolism, signaling and nutrient connections (2026-09-17) · lines 1334–1345

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetic screens, cancer models and patient-derived xenografts · source_derived_draft · unverified_draft

    ### glutathione-primary-tumor-null Primary tumor growth was unaffected by A39 loss in the reported comparison. Condition category: normal nutrient_topic: Glutathione research collection; topical membership is not evidence of a direct dietary effect. plain_language: Early colonization and growth of the original tumor were distinct endpoints. organism: Experimental breast-cancer cells and mouse xenografts tissue_or_cell_type: Early lung metastatic colonization experimental_model: Genetic screens, cancer models and patient-derived xenografts limitations: Cancer-specific mechanism; no inference that dietary or supplemental GSH causes metastasis in people. exposure: SLC25A39 loss and ATF4 CRISPR activation evidence_span: {"source_cache": "artifacts/glutathione-research/40736010.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e", "start_char": 0, "end_char": 1513, "text_sha256": "6c5baf25f027a65c991f7d45f87238cad1e474e7e910dceb32aa78a108e6d29e"} [glutathione-p40736010] Mitochondrial Glutathione Import Enables Breast Cancer Metastasis via Integrated Stress Response Signaling. (2025). https://pubmed.ncbi.nlm.nih.gov/40736010/ DOI: 10.1158/2159-8290.cd-24-1556
    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