Component
GPX4 protein stability 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.
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 acts on it
APT2 knockdown increased GPX4 protein stability in A375 cycloheximide-chase experiments.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_cache
- artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc
- experimental_model
- Human A375 melanoma; lentiviral APT2 shRNA
- exposure
- Cycloheximide chase; three independent experiments; exact CHX concentration and time series not resolved from reviewed legend.
- 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 5i,j
- primary_references
- https://doi.org/10.1038/s41467-025-56344-5
- source_access
- Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis.
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
APT2: sulforaphane engagement, GPX4 stability and ZDHHC6 turnover · lines 118–126
Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human A375 melanoma; lentiviral APT2 shRNA · source_derived_draft · unverified_draft
APT2 knockdown increased GPX4 protein stability in A375 cycloheximide-chase experiments. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 5i,j source_access: Selected primary Results and Figure 5/6 legends reviewed. No supplement or raw-data reanalysis. evidence_cache: artifacts/discovery-research/round6-sources/gpx4-primary-passages.json; SHA256 384aaae29ec0e6fe9814782b3e5d885753751fa1b2bbd103e30e8ffa113df5dc experimental_model: Human A375 melanoma; lentiviral APT2 shRNA organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: Cycloheximide chase; three independent experiments; exact CHX concentration and time series not resolved from reviewed legend. 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
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.