Component
Human APT2/LYPLA2 knockdown in HEK293T
3 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
APT2 knockdown reduced nuclear p-STAT3 in the HEK293T fractionation experiment.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human HEK293T subcellular fractionation
- exposure
- LYPLA2 siRNA; exact dose/duration for this panel 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
- Figure 2g; 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 24–30
Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human HEK293T subcellular fractionation · source_derived_draft · unverified_draft
APT2 knockdown reduced nuclear p-STAT3 in the HEK293T fractionation experiment. primary_references: https://doi.org/10.1038/s41586-020-2799-2 primary_locator: Figure 2g; APT2 depalmitoylates p-STAT3. organism: Human experimental_model: Human HEK293T subcellular fractionation exposure: LYPLA2 siRNA; exact dose/duration for this panel 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 evidenceAPT2 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 evidenceLYPLA2 siRNA increased STAT3 palmitoylation in the reported reconstituted HEK293T experiment.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- experimental_model
- Human HEK293T; DHHC7 knockout reconstituted with HA-DHHC7 and Flag-STAT3; DHHC construct species is not established as human for this figure.
- exposure
- LYPLA2 siRNA before Alk14 labeling; Figure 2f states 36 hours before labeling; exact siRNA amount 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
- Figure 2f; Extended Data 7d.
- 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 15–21
Selected primary observations: 10.1038/s41586-020-2799-2 and 10.1038/s41388-020-1335-z. · supports · Human HEK293T; DHHC7 knockout reconstituted with HA-DHHC7 and Flag-STAT3; DHHC construct species is not established as human for this figure. · source_derived_draft · unverified_draft
LYPLA2 siRNA increased STAT3 palmitoylation in the reported reconstituted HEK293T experiment. primary_references: https://doi.org/10.1038/s41586-020-2799-2 primary_locator: Figure 2f; Extended Data 7d. organism: Human experimental_model: Human HEK293T; DHHC7 knockout reconstituted with HA-DHHC7 and Flag-STAT3; DHHC construct species is not established as human for this figure. exposure: LYPLA2 siRNA before Alk14 labeling; Figure 2f states 36 hours before labeling; exact siRNA amount 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.