Component

Membrane-to-cytosol APT2 ratio in human cells

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. Sulforaphane reduced the membrane-to-cytosol ratio of FLAG-tagged APT2 in HEK293 fractionation experiments.

    Experimental context and source evidence
    evidence_cache
    artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a
    experimental_model
    Human HEK293 expressing FLAG-tagged human APT2
    exposure
    100 micromolar sulforaphane for 3 hours; membrane and cytosol fractions with pan-cadherin and alpha-tubulin markers; three separate experiments.
    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. The authors describe plasma-membrane localization, but fractionation is not an ER-specific or organelle-resolved measurement.
    organism
    Human experimental cells; construct species unresolved where stated for discussion-only nulls
    primary_locator
    Figure 4A; Results 3.4 and Methods 2.9
    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 30–38

    Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human HEK293 expressing FLAG-tagged human APT2 · source_derived_draft · unverified_draft

    Sulforaphane reduced the membrane-to-cytosol ratio of FLAG-tagged APT2 in HEK293 fractionation experiments. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Figure 4A; Results 3.4 and Methods 2.9 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: Human HEK293 expressing FLAG-tagged human APT2 organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: 100 micromolar sulforaphane for 3 hours; membrane and cytosol fractions with pan-cadherin and alpha-tubulin markers; three separate experiments. 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. The authors describe plasma-membrane localization, but fractionation is not an ER-specific or organelle-resolved measurement.
    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