Component
Human APT2-C56S expressed in HEK293 with sulforaphane exposure
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
Sulforaphane did not significantly attenuate Alk14 labeling of APT2-C56S under the conditions that reduced labeling of wild-type APT2.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_cache
- artifacts/discovery-research/round6-sources/sulforaphane-apt2.pdf; SHA256 31e2993f88fe05eec199b9013173b29379b3346b9696ac766771173ddd0f181a
- experimental_model
- Human HEK293 expressing FLAG-tagged APT2-C56S
- exposure
- 100 micromolar sulforaphane for 3 hours followed by 50 micromolar Alk14 for 5 hours; 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. C56S is a mutant-plus-exposure actor. Its baseline function must be assessed before using it as a selective pharmacological rescue.
- organism
- Human experimental cells; construct species unresolved where stated for discussion-only nulls
- primary_locator
- Figure 4C
- 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.
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 41–49
Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human HEK293 expressing FLAG-tagged APT2-C56S · source_derived_draft · unverified_draft
Sulforaphane did not significantly attenuate Alk14 labeling of APT2-C56S under the conditions that reduced labeling of wild-type APT2. primary_references: https://doi.org/10.1016/j.bbrc.2024.150244 primary_locator: Figure 4C 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 APT2-C56S organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: 100 micromolar sulforaphane for 3 hours followed by 50 micromolar Alk14 for 5 hours; 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. C56S is a mutant-plus-exposure actor. Its baseline function must be assessed before using it as a selective pharmacological rescue.
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.