Component
STAT3-dependent transcriptional output 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 reduced STAT3 transcriptional activity in the reported HEK293T experiments.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human HEK293T
- exposure
- LYPLA2 siRNA; exact exposure unresolved.
- limitations
- Reported cellular result, not a GPX4 time-course experiment. Overexpressed DHHC constructs in much of the study are mouse proteins; human constructs are explicitly identified only where confirmed. APT2 depletion, selective inhibitor exposure and sulforaphane are different interventions.
- organism
- Human
- primary_locator
- Extended Data 7e-f and Results: APT2 depalmitoylates p-STAT3.
- primary_references
- https://doi.org/10.1038/s41586-020-2799-2
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
APT2-STAT3 cycling and a competing sulforaphane target route · lines 33–39
Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human HEK293T · source_derived_draft · unverified_draft
APT2 knockdown reduced STAT3 transcriptional activity in the reported HEK293T experiments. primary_references: https://doi.org/10.1038/s41586-020-2799-2 primary_locator: Extended Data 7e-f and Results: APT2 depalmitoylates p-STAT3. organism: Human experimental_model: Human HEK293T exposure: LYPLA2 siRNA; exact exposure unresolved. limitations: Reported cellular result, not a GPX4 time-course experiment. Overexpressed DHHC constructs in much of the study are mouse proteins; human constructs are explicitly identified only where confirmed. APT2 depletion, selective inhibitor exposure and sulforaphane are different interventions.
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.