Component
GPX4 mRNA abundance in human cells
2 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
STAT3 siRNA reduced GPX4 mRNA in the reported gallbladder cancer-cell experiments.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human NOZ and GBC-SD gallbladder cancer cells
- exposure
- siSTAT3 versus control; reciprocal STAT3 overexpression increased mRNA/protein in the same reported figure group. Transfection duration not independently resolved here.
- limitations
- Human cancer-cell experiments; no clinical or dietary inference. Solasonine exposure is not equivalent to APT2 depletion, ML349, or sulforaphane. Mutant rescue does not by itself establish selectivity or normal baseline mutant function. Figure 5C calls this APT2 activity, but Methods 2.17 describes an anti-LYPLA2 ELISA with mass-concentration standards and an HRP/TMB readout from cell supernatants. No direct APT2 substrate-turnover assay is described there. The result is retained as an author-labelled activity proxy, not established catalytic inhibition. This methodological qualification does not invalidate the separately reported binding or cellular observations.
- organism
- Human
- primary_locator
- Figure 3A-D and Supplementary Figure S3A-B; Results 3.3.
- primary_references
- https://doi.org/10.1002/ptr.70245
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 141–147
Primary observations: 10.1038/s41467-025-56344-5 and 10.1002/ptr.70245; selected full-text review 2026-09-20. · supports · Human NOZ and GBC-SD gallbladder cancer cells · source_derived_draft · unverified_draft
STAT3 siRNA reduced GPX4 mRNA in the reported gallbladder cancer-cell experiments. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 3A-D and Supplementary Figure S3A-B; Results 3.3. organism: Human experimental_model: Human NOZ and GBC-SD gallbladder cancer cells exposure: siSTAT3 versus control; reciprocal STAT3 overexpression increased mRNA/protein in the same reported figure group. Transfection duration not independently resolved here. limitations: Human cancer-cell experiments; no clinical or dietary inference. Solasonine exposure is not equivalent to APT2 depletion, ML349, or sulforaphane. Mutant rescue does not by itself establish selectivity or normal baseline mutant function. Figure 5C calls this APT2 activity, but Methods 2.17 describes an anti-LYPLA2 ELISA with mass-concentration standards and an HRP/TMB readout from cell supernatants. No direct APT2 substrate-turnover assay is described there. The result is retained as an author-labelled activity proxy, not established catalytic inhibition. This methodological qualification does not invalidate the separately reported binding or cellular observations.
Complete structured claim and evidenceAPT2 knockdown did not significantly change GPX4 mRNA in the reported A375 and HT1080 RT-qPCR 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 and HT1080 cancer cells; lentiviral APT2 shRNA
- exposure
- RT-qPCR; three independent experiments; exposure timing unresolved.
- 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 actor names the A375 arm; the parallel HT1080 observation is preserved in the context. No transcriptional effect is inferred.
- organism
- Human experimental cells; construct species unresolved where stated for discussion-only nulls
- primary_locator
- Figure 5f
- 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 129–137
Targeted primary-literature curation from recursive ZDHHC6 exploration, 2026-09-20. · supports · Human A375 and HT1080 cancer cells; lentiviral APT2 shRNA · source_derived_draft · unverified_draft
APT2 knockdown did not significantly change GPX4 mRNA in the reported A375 and HT1080 RT-qPCR experiments. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 5f 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 and HT1080 cancer cells; lentiviral APT2 shRNA organism: Human experimental cells; construct species unresolved where stated for discussion-only nulls exposure: RT-qPCR; three independent experiments; exposure timing unresolved. 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 actor names the A375 arm; the parallel HT1080 observation is preserved in the context. No transcriptional effect is inferred.
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.