Component

Solasonine

10 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 it acts on

  1. Surface plasmon resonance reported solasonine binding to recombinant APT2, KD 2.982 micromolar.

    Solasonine → LYPLA2 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Recombinant human APT2 SPR; supporting cellular CETSA in NOZ/GBC-SD
    exposure
    SPR binding concentration series; cellular CETSA used 25 micromolar solasonine. Binding does not specify catalytic inhibition.
    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 5J and Methods 2.20; CETSA Figure 5F-G.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 60–66

    Primary observations: 10.1038/s41467-025-56344-5 and 10.1002/ptr.70245; selected full-text review 2026-09-20. · supports · Recombinant human APT2 SPR; supporting cellular CETSA in NOZ/GBC-SD · source_derived_draft · unverified_draft

    Surface plasmon resonance reported solasonine binding to recombinant APT2, KD 2.982 micromolar. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 5J and Methods 2.20; CETSA Figure 5F-G. organism: Human experimental_model: Recombinant human APT2 SPR; supporting cellular CETSA in NOZ/GBC-SD exposure: SPR binding concentration series; cellular CETSA used 25 micromolar solasonine. Binding does not specify catalytic inhibition. 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

  2. The study reports a reduced LYPLA2 ELISA signal as reduced APT2 activity; the described assay does not establish catalytic turnover.

    Solasonine → LYPLA2 antibody ELISA signal in human cell supernatants source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human NOZ and GBC-SD gallbladder cancer cells
    exposure
    Cell-supernatant ELISA; 0-50 ng/mL standards, anti-LYPLA2 plates, LYPLA2-HRP conjugate, H2O2/TMB chromogen, 450 nm readout with 630 nm reference. Cellular drug duration described as 48 hours.
    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 5C versus Methods 2.17 ELISA Assay.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 105–111

    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

    The study reports a reduced LYPLA2 ELISA signal as reduced APT2 activity; the described assay does not establish catalytic turnover. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 5C versus Methods 2.17 ELISA Assay. organism: Human experimental_model: Human NOZ and GBC-SD gallbladder cancer cells exposure: Cell-supernatant ELISA; 0-50 ng/mL standards, anti-LYPLA2 plates, LYPLA2-HRP conjugate, H2O2/TMB chromogen, 450 nm readout with 630 nm reference. Cellular drug duration described as 48 hours. 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

  3. Solasonine did not change APT2 protein expression in the reported immunoblots.

    Solasonine → APT2 protein 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 5B; Supplementary Figure S4B; Results 3.5.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 96–102

    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 did not change APT2 protein expression in the reported immunoblots. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 5B; Supplementary Figure S4B; Results 3.5. 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

  4. Solasonine reduced APT2-STAT3 co-immunoprecipitation.

    Solasonine → APT2-STAT3 co-immunoprecipitation in human cells source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human NOZ and GBC-SD gallbladder cancer cells
    exposure
    25 micromolar solasonine; main methods specify 48-hour cellular drug exposure.
    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 5D-E; Results 3.5.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 114–120

    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 APT2-STAT3 co-immunoprecipitation. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 5D-E; Results 3.5. organism: Human experimental_model: Human NOZ and GBC-SD gallbladder cancer cells exposure: 25 micromolar solasonine; main methods specify 48-hour cellular drug exposure. 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

  5. Solasonine suppressed STAT3-driven GPX4 wild-type promoter reporter activity; binding-motif mutations abolished the reported responses.

    Solasonine → GPX4 promoter luciferase activity 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 3I; Results 3.3; ChIP evidence in Figure 3E-H.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 123–129

    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 suppressed STAT3-driven GPX4 wild-type promoter reporter activity; binding-motif mutations abolished the reported responses. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 3I; Results 3.3; ChIP evidence in Figure 3E-H. 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

  6. Solasonine suppressed STAT3-driven SLC7A11 wild-type promoter reporter activity; binding-motif mutations abolished the reported responses.

    Solasonine → SLC7A11 promoter luciferase activity 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 3I; Results 3.3; ChIP evidence in Figure 3E-H.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 132–138

    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 suppressed STAT3-driven SLC7A11 wild-type promoter reporter activity; binding-motif mutations abolished the reported responses. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 3I; Results 3.3; ChIP evidence in Figure 3E-H. 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

  7. 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

  8. Solasonine increased STAT3 acyl-biotin-exchange signal.

    Solasonine → STAT3 palmitoylation 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 5A; Supplementary Figure S4A; Results 3.5.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 69–75

    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 increased STAT3 acyl-biotin-exchange signal. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 5A; Supplementary Figure S4A; Results 3.5. 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

  9. Solasonine did not change whole-cell phosphorylated STAT3 in the reported immunoblots.

    Solasonine → Whole-cell 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 4A; Results 3.4.
    primary_references
    https://doi.org/10.1002/ptr.70245

    APT2, STAT3 and GPX4: opposing branches and assay qualification · lines 87–93

    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 did not change whole-cell phosphorylated STAT3 in the reported immunoblots. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 4A; 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

Where it participates (unsigned role)

  1. Solasonine did not increase STAT3 palmitoylation in the reported APT2-D13A/L11A mutant setting.

    APT2-D13A/L11A expression with solasonine in human gallbladder cancer cells → STAT3 palmitoylation in human cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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 6E; Supplementary Figure S5A; Results 3.6.
    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 159–165

    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 did not increase STAT3 palmitoylation in the reported APT2-D13A/L11A mutant setting. primary_references: https://doi.org/10.1002/ptr.70245 primary_locator: Figure 6E; Supplementary Figure S5A; Results 3.6. 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.

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