Component

Nuclear phosphorylated STAT3 abundance in human cells

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. APT2 knockdown reduced nuclear p-STAT3 in the HEK293T fractionation experiment.

    Human APT2/LYPLA2 knockdown in HEK293T → Nuclear phosphorylated STAT3 abundance in human cells source_derived_draftungraded
    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 evidence

  2. Solasonine reduced nuclear phosphorylated STAT3, with cytoplasmic accumulation.

    Solasonine → Nuclear phosphorylated STAT3 abundance in human cells source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human NOZ and GBC-SD gallbladder cancer cells
    exposure
    Methods 2.2 describes 48-hour cellular drug treatments with refresh at 24 hours; exact concentration must be checked per figure and is not inferred from another assay.
    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 4B-D; Results 3.4.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 78–84

    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

    Solasonine reduced nuclear phosphorylated STAT3, with cytoplasmic accumulation. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 4B-D; Results 3.4. organism: Human experimental_model: Human NOZ and GBC-SD gallbladder cancer cells exposure: Methods 2.2 describes 48-hour cellular drug treatments with refresh at 24 hours; exact concentration must be checked per figure and is not inferred from another assay. 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 evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards