Component

ER-mitochondria contacts in human cells

3 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. 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

  2. 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

  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.

    Evidence, AI assistance and curation standards