Component

Oxidative-stress resistance

Experimental ability to withstand oxidant exposure.

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

What acts on it

  1. Experimental cells lacking FTSJ1 become more sensitive to oxidative stress.

    FTSJ1 → Oxidative-stress resistance source_derived_draftsource_reported: Cell/biochemical and animal xenograft; a narrow primary-study spot check supports the named FTSJ1 finding.
    Experimental context and source evidence
    availability_state
    Experimental loss of FTSJ1-dependent tRNA modification.
    experimental_scope
    Cell/biochemical studies and melanoma xenograft models reported in the 2024 FTSJ1 study.
    limitations
    FTSJ1 loss is a machinery perturbation, not itself a nutritional selenium-deficiency syndrome. The results do not prove that Um34 determines every selenoprotein phenotype.
    trigger_kind
    machinery_impairment

    Selenium deficiency: a mechanism-first reference · lines 75–75

    Supplied selenium deficiency reference · supports · Supplied reference; verify the primary study and experimental context. · source_derived_draft · unverified_draft

    Update: FTSJ1 was identified in 2024 as the tRNA^[Ser]Sec Um34 methyltransferase. Loss of FTSJ1 reduced efficient Sec insertion and sensitized experimental cells to oxidative stress. Evidence: cell/biochemical and melanoma xenograft models. [1]
    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