Component
Human APT2-C2S 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Palmitoylation-deficient APT2-C2S overexpression did not reproduce the significant reduction in ZDHHC6 palmitoylation caused by wild-type APT2.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_cache
- artifacts/discovery-research/round6-sources/zdhhc6-primary-passages.json; SHA256 a02040bb8922a9170e095cdfb5e875a5e7f513b682c0ec69c19feacb3dc191b0
- experimental_model
- Human HeLa; tagged human APT2-C2S 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. This mutant result supports a role for APT2 palmitoylation in this substrate assay; it is not a sulforaphane experiment.
- 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.
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 85–93
Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human HeLa; tagged human APT2-C2S and ZDHHC6 constructs · source_derived_draft · unverified_draft
Palmitoylation-deficient APT2-C2S overexpression did not reproduce the significant reduction in ZDHHC6 palmitoylation caused by wild-type APT2. 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-C2S 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. This mutant result supports a role for APT2 palmitoylation in this substrate assay; it is not a sulforaphane experiment.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.