Component

Human APT2 wild-type overexpression in HeLa

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 it acts on

  1. Wild-type APT2 overexpression reduced radiolabeled palmitate incorporation into ZDHHC6 in HeLa cells.

    Experimental context and source evidence
    evidence_cache
    artifacts/discovery-research/round6-sources/zdhhc6-primary-passages.json; SHA256 a02040bb8922a9170e095cdfb5e875a5e7f513b682c0ec69c19feacb3dc191b0
    experimental_model
    Human HeLa; tagged human APT2 and ZDHHC6 constructs
    exposure
    24-hour plasmid expression, then 2-hour tritiated-palmitate labeling; normalized to ZDHHC6 protein; n=6.
    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.
    organism
    Human experimental cells; construct species unresolved where stated for discussion-only nulls
    primary_locator
    Figure 2E,F; Rapid APT2-mediated ZDHHC6 depalmitoylation
    primary_references
    https://doi.org/10.7554/eLife.27826
    source_access
    Selected primary Results, figure legends and methods via indexed publisher text. No supplement or raw-data reanalysis.

    APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 74–82

    Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human HeLa; tagged human APT2 and ZDHHC6 constructs · source_derived_draft · unverified_draft

    Wild-type APT2 overexpression reduced radiolabeled palmitate incorporation into ZDHHC6 in HeLa cells. primary_references: https://doi.org/10.7554/eLife.27826 primary_locator: Figure 2E,F; Rapid APT2-mediated ZDHHC6 depalmitoylation source_access: Selected primary Results, figure legends and methods via indexed publisher text. No supplement or raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/zdhhc6-primary-passages.json; SHA256 a02040bb8922a9170e095cdfb5e875a5e7f513b682c0ec69c19feacb3dc191b0 experimental_model: Human HeLa; tagged human APT2 and ZDHHC6 constructs organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: 24-hour plasmid expression, then 2-hour tritiated-palmitate labeling; normalized to ZDHHC6 protein; n=6. 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.
    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