Component

Ribosome stalling at GPX4 UGA

Failed or delayed GPX4 selenocysteine decoding under the specified cellular perturbation.

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. LRP8 loss caused GPX4 UGA-associated ribosome stalling in the tested cancer cells.

    ApoER2 / LRP8 → Ribosome stalling at GPX4 UGA source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    cancer cell lines
    experimental_model
    Genetic disruption and ribosome analyses
    limitations
    Tumor-cell result; GPX4 priority is context dependent.
    organism
    human

    Selenium: literature corrections and mechanism additions · lines 594–604

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Genetic disruption and ribosome analyses · secondary_verified · secondary_verified

    ## lrp8-loss-promotes-gpx4-stalling Disrupted selenium uptake hindered GPX4 production in these cancer cells. LRP8 loss caused GPX4 UGA-associated ribosome stalling in the tested cancer cells. Organism: human Cell type: cancer cell lines Experimental model: Genetic disruption and ribosome analyses Limitations: Tumor-cell result; GPX4 priority is context dependent. Primary reference: [Ribosome stalling during selenoprotein translation exposes a ferroptosis vulnerability](https://pubmed.ncbi.nlm.nih.gov/35637349/)
    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