Component

H-Ras palmitoylation in the sulforaphane null-result report

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. The sulforaphane study reports no significant change in H-Ras palmitoylation in the presence of sulforaphane.

    Experimental context and source evidence
    evidence_cache
    artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a
    experimental_model
    Cell model and construct species not specified for this discussion-only result
    exposure
    Dose, timing and assay details for this null result are not separately reported.
    limitations
    These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. No plotted experiment or effect-size interval is provided. This limits a universal APT2-substrate prediction.
    organism
    Human experimental cells; construct species unresolved where stated for discussion-only nulls
    primary_locator
    Discussion, page 6
    primary_references
    https://doi.org/10.1016/j.bbrc.2024.150244
    source_access
    Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis.

    APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 63–71

    Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Cell model and construct species not specified for this discussion-only result · source_derived_draft · unverified_draft

    The sulforaphane study reports no significant change in H-Ras palmitoylation in the presence of sulforaphane. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Discussion, page 6 source_access: Full six-page primary PDF, methods and discussion read; Figure 4 visually inspected. No raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a experimental_model: Cell model and construct species not specified for this discussion-only result organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: Dose, timing and assay details for this null result are not separately reported. limitations: These are separate experimental observations, not a demonstrated sulforaphane-GPX4-ZDHHC6 pathway. Sulforaphane-driven APT2 relocalization is not equivalent to genetic depletion or general catalytic inhibition. No dietary, clinical or selenium-repletion effect is inferred. Protein stability, palmitoylation and substrate output remain different measurements. No plotted experiment or effect-size interval is provided. This limits a universal APT2-substrate prediction.
    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