Component
Human A375 APT2 knockdown with HA-APT2 WT re-expression
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 it acts on
Wild-type APT2 re-expression restored RSL3 susceptibility in APT2-depleted A375 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human A375 melanoma cells with APT2 shRNA and lentiviral rescue constructs
- exposure
- HA-tagged rescue constructs; Figure 6j: 48-hour RSL3 challenge, n=3 independent experiments. Exact RSL3 concentrations follow the figure dose response and are not inferred here.
- limitations
- C2S affects APT2 palmitoylation/localization and is not identical to the S122A catalytic-site perturbation. Null comparisons do not prove equivalence. No sulforaphane or solasonine tested in this rescue experiment.
- organism
- Human
- primary_locator
- Figure 6i-j; Results: Inhibition of APT2 suppresses ferroptosis.
- primary_references
- https://doi.org/10.1038/s41467-025-56344-5
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 15–21
Primary observations: 10.1038/s41467-025-56344-5 and 10.1002/ptr.70245; selected full-text review 2026-09-20. · supports · Human A375 melanoma cells with APT2 shRNA and lentiviral rescue constructs · source_derived_draft · unverified_draft
Wild-type APT2 re-expression restored RSL3 susceptibility in APT2-depleted A375 cells. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 6i-j; Results: Inhibition of APT2 suppresses ferroptosis. organism: Human experimental_model: Human A375 melanoma cells with APT2 shRNA and lentiviral rescue constructs exposure: HA-tagged rescue constructs; Figure 6j: 48-hour RSL3 challenge, n=3 independent experiments. Exact RSL3 concentrations follow the figure dose response and are not inferred here. limitations: C2S affects APT2 palmitoylation/localization and is not identical to the S122A catalytic-site perturbation. Null comparisons do not prove equivalence. No sulforaphane or solasonine tested in this rescue experiment.
Complete structured claim and evidenceWild-type APT2 re-expression lowered GPX4 protein in APT2-depleted A375 cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human A375 melanoma cells with APT2 shRNA and lentiviral rescue constructs
- exposure
- HA-tagged rescue constructs; Figure 6j: 48-hour RSL3 challenge, n=3 independent experiments. Exact RSL3 concentrations follow the figure dose response and are not inferred here.
- limitations
- C2S affects APT2 palmitoylation/localization and is not identical to the S122A catalytic-site perturbation. Null comparisons do not prove equivalence. No sulforaphane or solasonine tested in this rescue experiment.
- organism
- Human
- primary_locator
- Figure 6i-j; Results: Inhibition of APT2 suppresses ferroptosis.
- primary_references
- https://doi.org/10.1038/s41467-025-56344-5
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 6–12
Primary observations: 10.1038/s41467-025-56344-5 and 10.1002/ptr.70245; selected full-text review 2026-09-20. · supports · Human A375 melanoma cells with APT2 shRNA and lentiviral rescue constructs · source_derived_draft · unverified_draft
Wild-type APT2 re-expression lowered GPX4 protein in APT2-depleted A375 cells. primary_references: https://doi.org/10.1038/s41467-025-56344-5 primary_locator: Figure 6i-j; Results: Inhibition of APT2 suppresses ferroptosis. organism: Human experimental_model: Human A375 melanoma cells with APT2 shRNA and lentiviral rescue constructs exposure: HA-tagged rescue constructs; Figure 6j: 48-hour RSL3 challenge, n=3 independent experiments. Exact RSL3 concentrations follow the figure dose response and are not inferred here. limitations: C2S affects APT2 palmitoylation/localization and is not identical to the S122A catalytic-site perturbation. Null comparisons do not prove equivalence. No sulforaphane or solasonine tested in this rescue 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.