Component

Human MITOL / MARCHF5 / MARCH5

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

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

Where it participates (unsigned role)

  1. VAPB knockdown reduced MITOL-mediated HMOX2 ubiquitination in HeLa cells.

    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/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    48-hour siRNA exposure; indicated vectors transfected 20 hours before IP-immunoblot; siRNA concentration 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 2e; Results on MERCs integrity
    primary_references
    https://doi.org/10.1038/s41556-026-01974-0

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 50–58

    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 MITOL-mediated HMOX2 ubiquitination in HeLa cells. primary_references: https://doi.org/10.1038/s41556-026-01974-0 primary_locator: Figure 2e; Results on MERCs integrity evidence_cache: artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a 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: 48-hour siRNA exposure; indicated vectors transfected 20 hours before IP-immunoblot; siRNA concentration 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