Component

SLC25A39 knockdown in HeLa cells

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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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.

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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. SLC25A39 knockdown increased ER-mitochondria contacts in HeLa MERBiT cells.

    SLC25A39 knockdown in HeLa cells → ER-mitochondria contacts in human cells source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    3-day siRNA exposure; MERBiT luminescence; dose unresolved
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Figure 2f and Results: Induction of mitochondrial ROS
    primary_references
    https://doi.org/10.1038/s41467-025-56666-4

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 6–14

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    SLC25A39 knockdown increased ER-mitochondria contacts in HeLa MERBiT cells. primary_references: https://doi.org/10.1038/s41467-025-56666-4 primary_locator: Figure 2f and Results: Induction of mitochondrial ROS evidence_cache: artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6 access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: 3-day siRNA exposure; MERBiT luminescence; dose unresolved limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. RMDN3 knockdown reduced the increased contacts observed during SLC25A39 knockdown.

    RMDN3 knockdown in human cells → ER-mitochondria contacts in human cells source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    HeLa MERBiT cells; combined knockdown; exact supplementary timing/dose unresolved
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Results citing Supplementary Figure 4a
    primary_references
    https://doi.org/10.1038/s41467-025-56666-4

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 17–25

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    RMDN3 knockdown reduced the increased contacts observed during SLC25A39 knockdown. primary_references: https://doi.org/10.1038/s41467-025-56666-4 primary_locator: Results citing Supplementary Figure 4a evidence_cache: artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6 access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: HeLa MERBiT cells; combined knockdown; exact supplementary timing/dose unresolved limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    Complete structured claim and evidence

  2. RMDN3 knockdown reduced HeLa cell viability during SLC25A39 silencing.

    RMDN3 knockdown in human cells → HeLa cell viability readout source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    Combined silencing; CCK-8 viability assay; exact supplementary dose and timing unresolved
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Results: Disruption of mitochondrial ROS-derived MERCs; Supplementary Figure 5a
    primary_references
    https://doi.org/10.1038/s41467-025-56666-4

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 39–47

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    RMDN3 knockdown reduced HeLa cell viability during SLC25A39 silencing. primary_references: https://doi.org/10.1038/s41467-025-56666-4 primary_locator: Results: Disruption of mitochondrial ROS-derived MERCs; Supplementary Figure 5a evidence_cache: artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6 access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: Combined silencing; CCK-8 viability assay; exact supplementary dose and timing unresolved limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    Complete structured claim and evidence

  3. VAPB knockdown reduced the increased contacts observed during SLC25A39 knockdown.

    VAPB knockdown in human cells → ER-mitochondria contacts in human cells source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    HeLa MERBiT cells; combined knockdown; exact supplementary timing/dose unresolved
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Results citing Supplementary Figure 4a
    primary_references
    https://doi.org/10.1038/s41467-025-56666-4

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 28–36

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    VAPB knockdown reduced the increased contacts observed during SLC25A39 knockdown. primary_references: https://doi.org/10.1038/s41467-025-56666-4 primary_locator: Results citing Supplementary Figure 4a evidence_cache: artifacts/discovery-research/round4-sources/contact-2025-indexed-passages.json; SHA256 9222f94099520a9b5e9ee8b7f30a1b4ae261735d37462b13d7ca3d0ecc8792d6 access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: HeLa MERBiT cells; combined knockdown; exact supplementary timing/dose unresolved limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    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.

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